Cell-type specific interaction of endothelin and the nitric oxide system: pattern of prepro-ET1 expression in kidneys of L-NAME treated prepro-ET1 promoter-lacZ-transgenic mice.

  • Nitric oxide (NO) and endothelin-1 (ET-1) are known to play a major role in renal and vascular pathophysiology and exhibit a close interaction with ET-1, stimulating NO production; NO in turn inhibits ET-1 expression. Our objectives were (1) to establish a novel transgenic mouse model facilitating ET-1 expression assessment in vivo, (2) to validate this model by assessing prepro-ET-1 promoter activity in mice embryos by means of our novel model and comparing expression sites to well-established data on ET-1 in fetal development and (3) to investigate renal ET-NO interaction by assessing prepro-ET-1 promoter activity in different structures of the renal cortex in the setting of blocked NO synthases via L-NAME administration. We established transgenic mice carrying a lacZ reporter gene under control of the human prepro-ET-1 gene promoter sequence (8 kb of 5′ sequences).
  • Bluo-Gal staining of tissue sections revealed intracellular blue particles as indicators of prepro-ET-1 promoter activity. In mouse embryos, we detected high prepro-ET-1 promoter activity in the craniofacial region, as well as in bone and cartilage consistent with the literature. In order to investigate the interaction of ET-1 and NO in the kidney in vivo, transgenic mice at the age of 3-4 months were treated with a single dose of the NO synthase inhibitor L-NAME (25 mg (kg bw)(-1) i.p.) 12 h before kidney removal. Bluo-Gal staining of kidney sections revealed intracellular blue particles as indicators of prepro-ET-1 promoter activity in tubular and vascular endothelium and glomerular cells.
  • Particle count was closely correlated to kidney tissue ET-1 content (R=0.918, P<0.001). Comparison of counts revealed an increase by 135+/-53% in L-NAME treated (n=12) compared to non-treated mice (n=10, P=0.001). Cell-type specific evaluation revealed an increase of 136+/-51% in tubular (P=0.001) and 105+/-41% in glomerular cells (P=0.046), but no significant increase in vascular endothelium. In conclusion, our study revealed a close interaction of renal endothelin and the NO system in a cell-type specific manner. Our new transgenic model provides a unique opportunity to analyse regulation of the ET system on a cellular level in vivo.

<em>Endothelin</em>-<em>1</em> promotes cell survival in renal cell carcinoma through the <em>ET</em>(A) receptor.

Endothelin-1 (ET-1) is a potent vasoconstrictor that has been shown to significantly impact many benign and malignant tissues by signaling through its two cognate receptors: ET(A) and ET(B). As ET-1 has a role in both normal and diseased kidney, we initiated studies to investigate endothelin axis expression and function in renal cell carcinoma (RCC). In this study, relatively high levels of ET-1 were detected in all six human RCC cell lines investigated. RT-PCR and Southern analyses revealed that all six RCC cell lines expressed ET(A) receptor mRNA, while 3/6 cell lines also expressed ET(B) mRNA.
High affinity ET-1 binding occurred in all but one RCC cell line and quantitative RT-PCR demonstrated ET(A) mRNA expression in all six cell lines. Methylation of the ET(B) promoter (EDNRB) in 4/6 RCC cell lines was observed, suggesting a mechanism for repressed ET(B) expression. Moreover, methylation occurred in 32/48 of renal tumors and in 27/55 of histologically normal adjacent tissue samples studied, while no methylation was evident in any normal tissue isolated from nephrectomy or at autopsy. Functionally, ET-1 significantly inhibited paclitaxel-induced apoptosis in RCC cells through binding ET(A) with the ET-1 signaling mediated via the PI3-kinase/Akt pathway. Collectively, these data support the therapeutic targeting of the ET(A) receptor as a novel treatment strategy for RCC.

<em>Endothelin</em>-<em>1</em> and its receptors <em>ET</em>(A) and <em>ET</em>(B) in drug-induced gingival overgrowth.

BACKGROUND
The purpose of this study was to study the expression of endothelin-1 (ET-1) and its receptors ETA and ETB in normal human gingiva and cyclosporin-induced gingival fibroblasts.
METHODS
Gingival samples were collected from eight normal healthy individuals, eight patients with periodontitis, and eight patients with cyclosporin A (CsA)-induced gingival overgrowth. Total RNA was extracted from tissue samples, and reverse transcriptase-polymerase chain reaction was performed for ET-1, ETA, and ETB. ET-1 protein was estimated from the tissues by enzyme-linked immunosorbent assay. The expression of ET-1 and its receptors was also examined in gingival fibroblast cells treated with CsA.
RESULTS
ET-1 mRNA expression was significantly higher in patients with CsA-induced gingival overgrowth (P <0.001) than in patients with periodontitis and the controls. ETA mRNA was expressed more than the ETB in all examined samples. In human gingival fibroblasts, ET-1 expression was increased with CsA incorporation compared to controls (P <0.001).
CONCLUSIONS
These results suggest that CsA can modulate the expression of ET-1 in gingival fibroblasts and CsA-induced gingival overgrowth.

Regulation and expression of <em>endothelin</em>-<em>1</em> (<em>ET</em>-<em>1</em>) and <em>ET</em>-receptors in rat epithelial cells of renal and intestinal origin.

  • The hormone endothelin-1 (ET-1) is involved in many functions of the kidney and intestine. In addition to its vasoactive and proliferative effects, ET-1 is involved in the maintenance of water and salt balance, and in drug excretion by influencing the activity of different transporters in the epithelial cells of these two organs. To study ET-1 function and its role in pathophysiological processes in epithelial cells in vitro, we investigated ET-1 and ET-receptor expression and inducibility of ET-1 excretion by cytokines in three rat cell lines of intestinal (IEC-6) and renal (NRK-52E and GERP) origin.
  • Immunocytochemistry showed that all three cell lines express ET-1 and the ET-A and ET-B receptor. ET-1 was expressed intracellularly, and also the ET-A receptor showed a punctate intracellular staining pattern. The ET-B receptor was localized in the membrane, which was confirmed by Western blot analysis. Real-time RT-PCR and ELISA showed that exposure of IEC-6 cells to the cytokines, interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNFalpha), induced ET-1 mRNA expression and excretion, while IL-2 was ineffective.
  • In NRK-52E cells, IL-1beta and TNFalpha induced ET-1 excretion as well. In GERP cells, adequate measurement of cytokine effects on ET-1 excretion was not possible, since ET-1 excretion under non-stimulated conditions was around the lowest level of detection. In conclusion, we showed ET-1 and ET-receptor expression, and inducibility of ET-1 by cytokines in IEC-6, NRK-52E, and GERP cells.
  • These rat intestinal and renal cell lines appear to be suitable for further characterisation of ET-1 function and its role in pathophysiological processes in epithelial cells.

Endothelin 1 (ET-1) Antibody

abx024086-100ug Abbexa 100 ug 1128 EUR

ET-1(Endothelin-1) ELISA Kit

EU0205 FN Test 96T 628.92 EUR

Rat Endothelin 1 (ET-1) CLIA Kit

abx195562-96tests Abbexa 96 tests 990 EUR

Porcine endothelin-1 (ET-1) ELISA Kit

QY-E40122 Qayee Biotechnology 96T 480 EUR

Rat Endothelin 1,ET-1 ELISA Kit

CN-01966R1 ChemNorm 96T 560.4 EUR

Pig endothelin 1, ET-1 ELISA Kit

CSB-E06806p-24T Cusabio 1 plate of 24 wells 198 EUR

Pig endothelin 1, ET-1 ELISA Kit

1-CSB-E06806p Cusabio
  • 964.80 EUR
  • 6118.80 EUR
  • 3244.80 EUR
  • 1 plate of 96 wells
  • 10 plates of 96 wells each
  • 5 plates of 96 wells each

rat Endothelin 1, ET-1 ELISA Kit

CSB-E06979r-24T Cusabio 1 plate of 24 wells 198 EUR

rat Endothelin 1, ET-1 ELISA Kit

1-CSB-E06979r Cusabio
  • 964.80 EUR
  • 6118.80 EUR
  • 3244.80 EUR
  • 1 plate of 96 wells
  • 10 plates of 96 wells each
  • 5 plates of 96 wells each

Dog Endothelin 1, ET-1 ELISA Kit

CSB-E07002c-24T Cusabio 1 plate of 24 wells 198 EUR

Dog Endothelin 1, ET-1 ELISA Kit

1-CSB-E07002c Cusabio
  • 964.80 EUR
  • 6118.80 EUR
  • 3244.80 EUR
  • 1 plate of 96 wells
  • 10 plates of 96 wells each
  • 5 plates of 96 wells each

Rat ET-1(Endothelin 1) ELISA Kit

ER0019 FN Test 96T 628.92 EUR

Rat Endothelin 1(ET-1)ELISA Kit

GA-E0470RT-48T GenAsia Biotech 48T 380.4 EUR

Rat Endothelin 1(ET-1)ELISA Kit

GA-E0470RT-96T GenAsia Biotech 96T 595.2 EUR

Rat Endothelin 1(ET-1)ELISA Kit

QY-E11182 Qayee Biotechnology 96T 433.2 EUR

Rat Endothelin 1,ET-1 ELISA Kit

YLA0332RA-48T Shanghai YL Biotech 48T 465 EUR

Rat Endothelin 1,ET-1 ELISA Kit

YLA0332RA-96T Shanghai YL Biotech 96T 600 EUR

Endothelin-1 (ET-1) ELISA Kit (1 Plate)

K045-H1 Arbor Assays 1x96 well plate 590 EUR

Human Endothelin 1 (ET-1) CLIA Kit

abx195560-96tests Abbexa 96 tests 990 EUR

Mouse Endothelin 1 (ET-1) CLIA Kit

abx195561-96tests Abbexa 96 tests 990 EUR

human Endothelin 1,ET-1 ELISA Kit

201-12-1239 SunredBio 96 tests 528 EUR

Mouse Endothelin 1,ET-1 ELISA Kit

CN-02844M1 ChemNorm 96T 526.8 EUR

Mouse Endothelin 1,ET-1 ELISA Kit

CN-02844M2 ChemNorm 48T 348 EUR

human Endothelin 1,ET-1 ELISA Kit

CN-04153H1 ChemNorm 96T 538.8 EUR

human Endothelin 1,ET-1 ELISA Kit

CN-04153H2 ChemNorm 48T 358.8 EUR

Mouse Endothelin 1, ET-1 ELISA Kit

CSB-E05145m-24T Cusabio 1 plate of 24 wells 198 EUR

[Relationship of <em>endothelin</em>-<em>1</em> (<em>ET</em>-<em>1</em>) TaqI and tumor necrosis factor (TNF) a gene polymorphism with portal hypertension in liver cirrhosis].

OBJECTIVE
To study whether liver cirrhosis and portal hypertension are associated with ET-1 TaqI polymorphism and TNFa promoter-308G to A polymorphism.
METHODS
A case control study of 106 patients with liver cirrhosis following HBV C infection was performed in comparison with 108 controls by PCR-RFLP.
RESULTS
The frequency of C allele and CC+TC genotype in TaqI polymorphism of ET-1 gene in the portal hypertension group (LC+) was significantly higher than that in the healthy controls, and the frequency of TNF2/1 genotype in TNFa promoter -308 G to A polymorphism in LC+ group was significantly higher than that in the control group. The results by stratification analysis showed that TCF2 genotype frequency was higher in the LC+ group than in the control group. ET-1 TaqI polymorphism and TNFa polymorphism were risk factors for the occurrence of portal hypertension by Logistic regression analysis.
CONCLUSIONS
ET-1 TaqI polymorphism and TNFa polymorphism are associated with portal hypertension, and are new risk factors for the occurrence of portal hypertension. TCF2 genotype may be a susceptible gene of portal hypertension.

Comparative Analysis between Urinary Calprotectin and Serum Creatinine for Early Detection of Intrinsic Acute Kidney Injury

Background: Acute kidney injury (AKI) is a common and important clinical condition that may lead to chronic kidney disease if it is not diagnosed and treated in its early stages. Urinary calprotectin is a valuable recognized biomarker that can be used to differentiate prerenal and intrinsic AKI. However, till date only a few reports on urine calprotectin measurement in early diagnosis of intrinsic AKI are available. In this study, we compared the sensitivity and specificity of urinary calprotectin with those of serum creatinine in detecting early intrinsic AKI.
Methods: Over 6 months period (April to October 2018), 81 of 408 patients admitted to the pediatric intensive care unit met the criteria of this cross-sectional study. Their serum creatinine and urinary calprotectin were measured on the first and third day of admission using Jaffe and Elisa radioimmunoassay methods, respectively. The AKI was defined according to the pRIFLE criteria.
Results: Of the total 81 patients, 67 had the criteria of intrinsic AKI. Of these 62% were female and 38% were male. The mean age of the patients was 22 months. According to data analysis, the area under the curve of ROC of urinary calprotectin on day-1 to detect renal failure is 0.93 with the best cutoff point obtained at 530 ng/mL. The sensitivity, specificity, positive, and negative predictive values of urinary calprotectin levels in diagnosing AKI at this cutoff point are 92.5%, 92.8%, 98.4, and 72.2%, respectively. Besides, urinary calprotectin changes occur much earlier than the rising of serum creatinine.
Conclusion: Urinary level of calprotectin is a very sensitive biomarker for early diagnosis of intrinsic AKI in children and it can be used in intensive care units or anywhere critically ill children admitted to detect intrinsic AKI. Besides, this study shows that urine calprotectin may be a more sensitive and specific biomarker than serum creatinine in the early phases of intrinsic AKI.

High-performance surface-enhanced Raman spectroscopy chip integrated with a micro-optical system for the rapid detection of creatinine in serum

To improve the sensitivity of disease biomarker detection, we proposed a high-performance surface-enhanced Raman spectroscopy (SERS) chip integrated with a micro-optical system (MOS). The MOS, which is based on the micro-reflecting cavity and the micro-lens, optimizes the optical matching characteristics of the SERS substrate and the Raman detection system, and greatly improves the SERS detection sensitivity by improving the collection efficiency of the Raman scattering signal. A uniform single layer of silver nanoparticles on a gold film was prepared as the SERS substrate using a liquid-liquid interface self-assembly method. The micro-reflecting cavity and micro-lens were prepared using micro-processing technology. The SERS chip was constructed based on the MOS and the Au film-based SERS substrate, and experimental results showed an EF of 1.46×108, which is about 22.4 times higher than that of the Si-based SERS substrate.
The chip was used for the detection of creatinine and the detection limit of creatinine in aqueous solution was 1 µM while the detection limit in serum was 5 µM. In addition, SERS testing was conducted on serum samples from normal people and patients with chronic renal impairment. Principal component analysis and linear discriminant analysis were used for modeling and identification, and the results showed a 90% accuracy of blind sample detection. These results demonstrate the value of this SERS chip for both research and practical applications in the fields of disease diagnosis and screening.

Drain fluid creatinine-to-serum creatinine ratio as an initial test to detect urine leakage following cystectomy: A retrospective study

Introduction: Urine leak following radical cystectomy is a known complication. Among the various methods to diagnose this, assessment of drain fluid creatinine is a relatively easy procedure. We aimed to ascertain the validity of the drain fluid creatinine-to-serum creatinine ratio (DCSCR) as an initial indicator of urinary leak in patients undergoing radical cystectomy.
Methods: We retrospectively identified consecutive patients with documentation of drain fluid creatinine in the postoperative period following cystectomy and urinary diversion at our institution between January 2009 and December 2018. All continent diversions and any patient with a DCSCR >1.5:1 underwent contrast study postoperatively. A diagnosis of urine leak was made following confirmatory imaging. Receiver operative characteristic curves were created, and Youden’s index was used to determine the strength and clinical utility of DCSCR as a diagnostic test.
Results: Two hundred forty-four of the 340 patients included in the study underwent cystectomy with conduit and 81 underwent neobladder creation. Sixteen out of 340 (4.7%) patients had radiologically confirmed urinary leak. DCSCR was elevated in all ureteric anastomotic leaks and in 1 out of the 7 neobladder-urethral anastomotic (NUA) leaks. The sensitivity and specificity of DCSCR to predict all urinary leaks were 68.8% and 80.9% at 1.12 (area under the curve [AUC] = 0.838), whereas at a value of 1.18 (AUC = 0.876) and with the exclusion of NUA leaks, the sensitivity was 77.8% and specificity was 87.6%.
Conclusions: DCSCR is a good preliminary test for identifying patients who need prompt confirmatory testing for localizing urinary leaks. A drain creatinine level just 18% higher than the serum creatinine level can signify a urine leak. This is different from general assumptions of a higher DCSCR.

Creatinine Serum Detection Kit

SKT-217-192 Stressmarq 2 plates of 96 wells 410.4 EUR

Urine Creatinine Detection Kit

SKT-200-192 Stressmarq 2 plates of 96 wells 410.4 EUR

Creatinine Urinary Detection Kit (2 Plate)

K002-H1 Arbor Assays 2x96 well plates 271 EUR

Creatinine Urinary Detection Kit (10 Plate)

K002-H5 Arbor Assays 10x96 well plates 949 EUR

Creatinine Serum Kit (2 Plate)

KB02-H1 Arbor Assays 2x96 well plates 277 EUR

Creatinine Serum Kit (4 Plate)

KB02-H2 Arbor Assays 4x96 well plates 454 EUR

DetectX® Creatinine Reagent, 20ML

C004-20ML Arbor Assays 20ML 254 EUR

DetectX® Creatinine Reagent, 50ML

C004-50ML Arbor Assays 50ML 360 EUR

Creatinine Serum Low Sample Volume Kit (384-well Plate)

KB02-H1D Arbor Assays 1x384 well plate 395 EUR

Serum Creatinine ELISA kit (colorimetric, all species), 96 tests, quantitative

100-300-SCR Alpha Diagnostics 1 kit 343.2 EUR

Serum Creatinine ELISA kit (colorimetric, all species), 2x96 tests, quantitative

100-305-SCR Alpha Diagnostics 1 kit 562.8 EUR

Creatinine

B1717-50 ApexBio 50 mg 153.6 EUR

Creatinine

CB0328 Bio Basic 5g 68.35 EUR

Creatinine

GK8780-100G Glentham Life Sciences 100 g 151.2 EUR

Creatinine

GK8780-25G Glentham Life Sciences 25 g 74.4 EUR

Creatinine

HY-B0504 MedChemExpress 500mg 129.6 EUR

Creatinine ELISA Kit| Mouse Creatinine ELISA Kit

EF013537 Lifescience Market 96 Tests 826.8 EUR

Human Urinary Creatinine(Urinary Creatinine) ELISA Kit

QY-E05390 Qayee Biotechnology 96T 433.2 EUR

Creatinine [BTG]

DAGA-186G Creative Diagnostics 500ug 1425.6 EUR

Creatinine-HRP

80-1133 Fitzgerald 500 ul 159.6 EUR

Creatinine-HRP

DAG-CL005 Creative Diagnostics 500 μl 1248 EUR

Potassium (Serum) Detection Assay Kit (Fluorometric)

K940-100 Biovision each 738 EUR

Creatinine(N) [HRP]

DAG1075 Creative Diagnostics 0.5ml 1014 EUR

Creatinine N-HRP

80-1132 Fitzgerald 500 ul 970.8 EUR

Creatinine Assay Kit

55R-1467 Fitzgerald 100 assays 765.6 EUR

Creatinine Assay Kit

abx098422-Hitachi7020R150ml3R250ml1 Abbexa Hitachi 7020; R1: 50ml×3 R2: 50ml×1 622.8 EUR

Creatinine Assay Kit

abx098422-Hitachi7060R190ml2R260ml1 Abbexa Hitachi 7060; R1: 90ml×2 R2: 60ml×1 566.4 EUR

Creatinine Assay Kit

abx098422-Toshiba120R140ml3R240ml1 Abbexa Toshiba 120; R1: 40ml×3 R2: 40ml×1 679.2 EUR

Utility of measuring serum creatinine to detect renal compromise in ED patients receiving IV contrast-enhanced CT scan

Objective: The objectives of this study are to determine the efficacy of a roster of clinical factors in identifying risk for renal insufficiency in emergency department (ED) patients requiring intravenous contrast-enhanced CT scan (IVCE-CT) and to help mitigate potential for developing contrast-induced nephropathy (CIN).
Methods: A review was conducted of consecutive ED patients who received IVCE-CT during a 4-month period in our urban ED. The values of ED serum creatinine (SCr) performed were tabulated. The medical records of all patients with an elevated SCr (> 1.4 mg/dL) were reviewed to determine and correlate the presence of clinical risk factors for underlying renal insufficiency.
Results: During the 4-month study period, there were 2260 consecutive cases who received IVCE-CT; of these, 2250 (99.6%) had concomitant measurement of SCr. Elevated SCr occurred in 141 patients (6.2%); of these, 75 had a SCr > 2 mg/dL. In all, 139/141 (98.6%) with an elevated SCr had an underlying chronic or acute medical condition identified by medical record review which potentially compromised renal function, including chronic renal disease, diabetes mellitus, HIV infection, cancer, hypertension, congestive heart failure, sepsis/septic shock, chronic alcoholism, and sickle cell disease. Two patients with no identified risk factor each had (mildly) elevated SCr; both had a normal SCr measured post-CT scan. The total cost of performing serum basic metabolic panel to measure SCr in all patients during the 4-month study period was $94,500.
Conclusions: Elevated SCr is rarely present in ED patients without recognized risk factors who receive IVCE-CT scan. The vast majority with underlying renal insufficiency are readily identified by a review of the patient’s medical history and/or clinical findings. Routine SCr measurement on all ED patients regardless of risk stratification prior to IVCE imaging is neither time nor cost-effective.

Telomere shortening is associated with corticosterone stress response in adult barn swallows

When vertebrates face stressful events, the hypothalamic-pituitary-adrenal (HPA) axis is activated, generating a rapid increase in circulating glucocorticoid (GC) stress hormones followed by a return to baseline levels. However, repeated activation of HPA axis may lead to increase in oxidative stress. One target of oxidative stress is telomeres, nucleoprotein complexes at the end of chromosomes that shorten at each cell division. The susceptibility of telomeres to oxidizing molecules has led to the hypothesis that increased GC levels boost telomere shortening, but studies on this link are scanty. We studied if, in barn swallows Hirundo rustica, changes in adult erythrocyte telomere length between 2 consecutive breeding seasons are related to corticosterone (CORT) (the main avian GC) stress response induced by a standard capture-restraint protocol.
Within-individual telomere length did not significantly change between consecutive breeding seasons. Second-year individuals showed the highest increase in circulating CORT concentrations following restraint. Moreover, we found a decline in female stress response along the breeding season. In addition, telomere shortening covaried with the stress response: a delayed activation of the negative feedback loop terminating the stress response was associated with greater telomere attrition. Hence, among-individual variation in stress response may affect telomere dynamics.

Context dependent variation in corticosterone and phenotypic divergence of Rana arvalis populations along an acidification gradient

Background: Physiological processes, as immediate responses to the environment, are important mechanisms of phenotypic plasticity and can influence evolution at ecological time scales. In stressful environments, physiological stress responses of individuals are initiated and integrated via the release of hormones, such as corticosterone (CORT). In vertebrates, CORT influences energy metabolism and resource allocation to multiple fitness traits (e.g. growth and morphology) and can be an important mediator of rapid adaptation to environmental stress, such as acidification. The moor frog, Rana arvalis, shows adaptive divergence in larval life-histories and predator defense traits along an acidification gradient in Sweden. Here we take a first step to understanding the role of CORT in this adaptive divergence. We conducted a fully factorial laboratory experiment and reared tadpoles from three populations (one acidic, one neutral and one intermediate pH origin) in two pH treatments (Acid versus Neutral pH) from hatching to metamorphosis. We tested how the populations differ in tadpole CORT profiles and how CORT is associated with tadpole life-history and morphological traits.
Results: We found clear differences among the populations in CORT profiles across different developmental stages, but only weak effects of pH treatment on CORT. Tadpoles from the acid origin population had, on average, lower CORT levels than tadpoles from the neutral origin population, and the intermediate pH origin population had intermediate CORT levels. Overall, tadpoles with higher CORT levels developed faster and had shorter and shallower tails, as well as shallower tail muscles.
Conclusions: Our common garden results indicate among population divergence in CORT levels, likely reflecting acidification mediated divergent selection on tadpole physiology, concomitant to selection on larval life-histories and morphology. However, CORT levels were highly environmental context dependent. Jointly these results indicate a potential role for CORT as a mediator of multi-trait divergence along environmental stress gradients in natural populations. At the same time, the population level differences and high context dependency in CORT levels suggest that snapshot assessment of CORT in nature may not be reliable bioindicators of stress.

RNA-seq based transcriptome analysis of ethanol extract of saffron protective effect against corticosterone-induced PC12 cell injury

Background: At present, oral antidepressants are commonly used in the clinical treatment of depression. However, the current drug treatment may lead to more serious adverse reactions. Therefore, we focus on Chinese traditional medicine, trying to find an effective and safe alternative or complementary medicine. Crocus sativus (saffron) is a traditional Chinese herbal medicine, which is typically used in the clinic to regulate anxiety, insomnia, amnesia, and other mental disorder. The study aimed to explore the neuroprotective effect of ethanol extract of saffron (EES) on corticosterone (CORT)- induced injury in PC12 cells and further explored its potential mechanism.
Methods: The authenticity of saffron and the active components of EES were identified by a water test and ultra-performance liquid chromatography-time of flight mass spectrometry system. The screening of cytotoxicity for PC12 cells was incubated with EES in different concentrations for 24 h, and the protective efficacy of EES on CORT (500 μM) -induced PC12 cell injury, cell viability was assessed by Cell Counting Kit-8 (CCK-8) assay. The differentially expressed genes (DEGs) of EES-protected PC12 cells were analyzed using the RNA-seq method, and the results were analyzed for GO and KEGG enrichment. The results of RNA-seq were verified by qPCR analysis.
Results: The saffron was initially identified as authentic in the water test and 10 compounds were identified by Ultra Performance Liquid Chromatography (UPLC)- Mass Spectrometry (MS). The results of CCK-8 demonstrated that EES at concentrations above 640 μg/mL exerted a certain cytotoxic effect, and PC12 cells pretreated with EES (20, 40, and 80 μg/mL) significantly reversed the 500 μM CORT-induced cell death. RNA-seq analysis showed that EES regulated 246 differential genes, which were mainly enriched in the MAPK signaling pathway. Dusp5, Dusp6, Gadd45b, Gadd45G, and Pdgfc were further validated by qPCR. Experimental data showed that the results of qPCR were consistent with RNA-seq.
Conclusions: These findings provide an innovative understanding of the molecular mechanism of the protective effect of EES on PC12 cells at the molecular transcription level, and Dusp5, Dusp6, Gadd45b, Gadd45g, and Pdgfc may be potential novel targets for antidepressant treatment.

Porcine corticosterone / corticosterone (CORT) ELISA Kit

QY-E40120 Qayee Biotechnology 96T 480 EUR

Corticosterone

B7469-5.1 ApexBio 10 mM (in 1mL DMSO) 129.6 EUR

Corticosterone

B7469-50 ApexBio 50 mg 142.8 EUR

Corticosterone

HY-B1618 MedChemExpress 10mM/1mL 151.2 EUR

Corticosterone

TBW01169 ChemNorm 20mg Ask for price

Corticosterone-BSA

80-1432 Fitzgerald 1 mg 781.2 EUR

Corticosterone-OVA

80-1433 Fitzgerald 1 mg 781.2 EUR

Corticosterone-BSA

80-1062 Fitzgerald 500 ug 360 EUR

Corticosterone-OVA

80-1063 Fitzgerald 500 ug 360 EUR

Corticosterone Antibody

10121-05011 AssayPro 150 ug 260.4 EUR

Corticosterone Antibody

10101-05011 AssayPro 150 ug 260.4 EUR

Corticosterone Antibody

40101-05011 AssayPro 150 ug 260.4 EUR

Corticosterone EIA Kit

SKT-205-96 Stressmarq 1 plate of 96 wells 426 EUR

Corticosterone ELISA kit

55R-IB79112 Fitzgerald 96 wells 694.8 EUR

Corticosterone Standard, 125UL

C151-125UL Arbor Assays 125UL 85 EUR

Corticosterone Standard, 625UL

C151-625UL Arbor Assays 625UL 207 EUR

Corticosterone Standard, 125UL

C043-125UL Arbor Assays 125UL 85 EUR

Corticosterone Standard, 625UL

C043-625UL Arbor Assays 625UL 207 EUR

Corticosterone (Cort) ELISA Kit

DLR-Cort-Ge-48T DL Develop 48T 562.8 EUR

Corticosterone (Cort) ELISA Kit

DLR-Cort-Ge-96T DL Develop 96T 729.6 EUR

Corticosterone (CORT) ELISA Kit

K4222-100 Biovision each 966 EUR

CORT(Corticosterone) ELISA Kit

EU3108 FN Test 96T 628.92 EUR

Rat Corticosterone ELISA kit

E02C0006-192T BlueGene 192 tests 1524 EUR

Rat Corticosterone ELISA kit

E02C0006-48 BlueGene 1 plate of 48 wells 624 EUR

Corticosterone and Adrenocorticotrophic Hormone Secretion Is Recovered after Immune Challenge or Acute Restraint Stress in Sepsis Survivor Animals

Background: Clinical and experimental studies report a dysregulation of hypothalamus-pituitary-adrenal (HPA) axis during sepsis that causes impairment in hormone secretion in the late phase contributing for the pathophysiology of the disease. However, it is unclear whether this alteration persists even after the disease remission.
Methods: We evaluated the effect of an immune challenge or restraint stress on the hormone secretion of HPA axis in sepsis survivor rats. Sepsis was induced by cecal ligation-puncture (CLP) surgery. Naive or animals that survive 5 or 10 days after CLP were submitted to lipopolysaccharide (LPS) injection or restraint stress. After 60 min, blood was collected for plasma nitrate, cytokines, adrenocorticotropic hormone (ACTH), and corticosterone (CORT) and brain for synaptophysin and hypothalamic cytokines.
Results: Five days survivor animals showed increased plasma nitrate (p < 0.001) and interleukin (IL)-1β levels (p < 0.05) that were abolished in the 10 days survivors. In the hypothalamus of both survivors, the reverse was seen with IL-6 increased (p < 0.01), while IL-1β did not show any alteration. Synaptophysin expression was reduced in both survivors and did not change after any stimuli. Only the LPS administration increased plasma and/or inflammatory mediators levels in both groups (survivors and naive) being apparently lower in the survivors. There was no difference in the increased secretion pattern of ACTH and CORT observed in the naive and sepsis survivor animals submitted to immune challenge or restraint stress.
Conclusion: We conclude that the HPA axis is already recovered soon after 5 days of sepsis induction responding with normal secretion of ACTH and CORT when required.

Coexistence of Renin-independent Aldosterone Secretion and Multiple Endocrine Neoplasia Type 1 Within a Family

Primary aldosteronism (PA) is a state of renin-independent aldosterone secretion that can range from subclinical to overt. Some normotensive individuals for whom PA screening is not routinely recommended are reported to fulfill the loading test criterion used for the diagnosis of PA. Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterized by the development of various endocrine tumors. Cases of PA associated with MEN1 have been reported; however, there has been no previous report on renin-independent aldosterone secretion within a family with MEN1. Herein, we present the case of a normotensive family presenting with both MEN1 and renin-independent aldosterone secretion. A 49-year-old man was admitted to our hospital for PA evaluation owing to the plasma aldosterone concentration/plasma renin activity ratio being greater than the screening cut-off value; the patient was normotensive.
The patient had a history of left nephrectomy and adrenalectomy for left renal carcinoma and adrenal tumor at the age of 39 years. Subsequently, he was diagnosed with MEN1 concurrent with primary hyperparathyroidism, insulinoma, and novel MEN1 gene mutations (c.655-5_655-4insC and c.818delC). The loading tests for PA confirmation, including saline infusion, and furosemide upright and captopril challenge tests, yielded positive findings, confirming a case of renin-independent aldosterone secretion. The patient’s mother, brother, and sister were also genetically or clinically diagnosed with MEN1. All of them were also normotensive and confirmed to have renin-independent aldosterone secretion. The coexistence of renin-independent aldosterone secretion and MEN1 within this family suggests a relationship between the 2 entities.

Compromised blood flow in the optic nerve head after systemic administration of 2 aldosterone in rats: A possible rat model of retinal ganglion cell loss

Purpose: To investigate the optic nerve head (ONH) blood flow, retinal vessel diameters, and retinal ganglion cell (RGC) loss after systemic administration of aldosterone in rats.
Methods: Aldosterone (80 μg/kg/day) or vehicle was administered using an osmotic minipump in Brown Norway rats. The mean blur rate in the vessel (MV) and tissue (MT) regions and retinal vessel diameters in the ONH were measured by laser speckle flowgraphy before and 1, 2, and 4 weeks after administration of aldosterone or vehicle. Intraocular pressure (IOP), blood pressure, and heart rate were recorded. The retrogradely labeled RGCs were counted in the retinal flatmounts prepared 5 weeks after treatment.
Results: The MV and MT in the aldosterone group significantly decreased at 2 and 4 weeks (MV: 2 weeks, P = 0.001, 4 weeks, P < 0.001; MT: 2 weeks, P = 0.02, 4 weeks, P = 0.03). The artery and vein diameters significantly decreased at 1, 2, and 4 weeks in the aldosterone group (all P < 0.001). The MV, MT, and vessel diameters remained unchanged in the vehicle group. Other parameters did not change over time in either group. RGC counts were significantly lower in the aldosterone group than in the vehicle group (P < 0.001).
Conclusions: ONH blood flow decreased following retinal vessel constriction without changes in IOP or blood pressure in a possible rat model of RGC loss by systemic administration of aldosterone.

Ocular Distribution of the Renin-Angiotensin-Aldosterone System in the Context of the SARS-CoV-2 Pandemic

The COVID-19 pandemic has resulted in an unprecedented impact on global health, economy, and way of life. SARS-CoV-2, the virus responsible for the disease, utilizes the ACE2 receptor found on host cells to mediate entry, replication, and infection. Numerous studies have elucidated the presence of many components of the renin-angiotensin-aldosterone system (RAAS) in the eye, including the ACE2 receptor. Considering this, and the anatomical vulnerability that the exposed ocular surface offers with its interconnectedness to the respiratory system, there is a theoretical risk of pathogen entry from the ocular route as well as the development of COVID-19-associated eye disease.
Despite this, the actual epidemiological data demonstrates low ocular symptoms, possibly due to differing ACE2 receptor expression across age, ethnicity, and sex coupled with the protective properties of tears. We summarize the current literature on ocular RAAS with specific focus on the ACE2 receptor and its interplay with the SARS-CoV-2 virus.

Report from the HarmoSter study: impact of calibration on comparability of LC-MS/MS measurement of circulating cortisol, 17OH-progesterone and aldosterone

Objectives: Liquid chromatography-tandem mass spectrometry (LC-MS/MS) is recommended for measuring circulating steroids. However, assays display technical heterogeneity. So far, reproducibility of corticosteroid LC-MS/MS measurements has received scant attention. The aim of the study was to compare LC-MS/MS measurements of cortisol, 17OH-progesterone and aldosterone from nine European centers and assess performance according to external quality assessment (EQA) materials and calibration.
Methods: Seventy-eight patient samples, EQA materials and two commercial calibration sets were measured twice by laboratory-specific procedures. Results were obtained by in-house (CAL1) and external calibrations (CAL2 and CAL3). We evaluated intra and inter-laboratory imprecision, correlation and agreement in patient samples, and trueness, bias and commutability in EQA materials.
Results: Using CAL1, intra-laboratory CVs ranged between 2.8-7.4%, 4.4-18.0% and 5.2-22.2%, for cortisol, 17OH-progesterone and aldosterone, respectively. Trueness and bias in EQA materials were mostly acceptable, however, inappropriate commutability and target value assignment were highlighted in some cases. CAL2 showed suboptimal accuracy. Median inter-laboratory CVs for cortisol, 17OH-progesterone and aldosterone were 4.9, 11.8 and 13.8% with CAL1 and 3.6, 10.3 and 8.6% with CAL3 (all p<0.001), respectively. Using CAL1, median bias vs. all laboratory-medians ranged from -6.6 to 6.9%, -17.2 to 7.8% and -12.0 to 16.8% for cortisol, 17OH-progesterone and aldosterone, respectively. Regression lines significantly deviated from the best fit for most laboratories. Using CAL3 improved cortisol and 17OH-progesterone between-method bias and correlation.
Conclusions: Intra-laboratory imprecision and performance with EQA materials were variable. Inter-laboratory performance was mostly within specifications. Although residual variability persists, adopting common traceable calibrators and RMP-determined EQA materials is beneficial for standardization of LC-MS/MS steroid measurements.

Aldosterone

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Aldosterone Antibody

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Aldosterone Antibody

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Aldosterone Antibody

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Aldosterone Antibody

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Aldosterone Antibody

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Aldosterone ELISA Kit

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Aldosterone 3 antibody

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Aldosterone (ALD) Antibody

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Aldosterone (ALD) Antibody

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Aldosterone (ALD) Antibody

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Aldosterone (ALD) Antibody

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Aldosterone (ALD) Antibody

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Aldosterone (ALD) Antibody

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Aldosterone Standard, 125UL

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Aldosterone Standard, 625UL

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Aldosterone (ALD) CLIA Kit

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  • 5095.20 EUR
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Aldosterone (ALD) ELISA Kit

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Aldosterone (ALD) ELISA Kit

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Aldosterone (ALD) ELISA Kit

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Aldosterone (ALD) ELISA Kit

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Aldosterone (ALD) ELISA Kit

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ALD(Aldosterone) ELISA Kit

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Dog Aldosterone ELISA kit

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Dog Aldosterone ELISA kit

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Dog Aldosterone ELISA kit

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High Prevalence of Autonomous Aldosterone Production in Hypertension: How to Identify and Treat It

Purpose of review: Primary aldosteronism (PA) affects millions of individuals worldwide. When unrecognized, PA leads to cardiovascular and renal complications via mechanisms independent from those mediated by hypertension. In this review, we emphasize the importance of PA screening in at-risk populations, and we provide options for customized PA therapy, with consideration for a variety of clinical care settings.
Recent findings: Compelling evidence puts PA at the forefront of secondary hypertension etiologies. Cardiovascular and renal damage likely begins in early stages of renin-independent aldosterone excess. PA must be considered not only in patients with resistant hypertension or hypokalemia, but also when hypertension is associated with obstructive sleep apnea or atrial fibrillation, or in those with early-onset hypertension. Screening with plasma aldosterone and renin is widely accessible, and targeted PA therapy can successfully circumvent the excess cardiorenal risk relative to equivalent primary hypertension. Identifying and treating PA in early stages provide opportunities for personalized hypertension therapy in a large number of patients. Additionally, early targeted therapy of PA is essential for pivoting the care of such patients from reactive to preventive of cardiovascular and renal morbidity and mortality.

Safety and Effectiveness of Oral Methylprednisolone Therapy in Comparison With Intramuscular Adrenocorticotropic Hormone and Oral Prednisolone in Children With Infantile Spasms

Background and Purpose: To assess the safety and effectiveness of oral methylprednisolone (oMP) in comparison with intramuscular adrenocorticotropic hormone (imACTH) and oral prednisolone (oP) therapies in children with infantile spasms (IS).
Methods: In this prospective, open-label, non-blinded, uncontrolled observational study, children (aged 2-24 months) with newly diagnosed IS presenting with hypsarrhythmia or its variants on electroencephalogram (EEG) were included. It was followed by imACTH, oP, or oMP (32-48 mg/day for 2 weeks followed by tapering) treatments. Electroclinical remission/spasm control, relapse, and adverse effects were evaluated in the short-term (days 14 and 42) and intermediary-term (3, 6, and 12 months) intervals.
Results: A total of 320 pediatric patients were enrolled: 108, 107, and 105 in the imACTH, oMP, and oP groups, respectively. The proportion of children achieving electroclinical remission on days 14 and 42 was similar among the three groups (day 14: 53.70 vs. 60.75 vs. 51.43%, p = 0.362; day 42: 57.55 vs. 63.46 vs. 55.34%, p = 0.470). The time to response was significantly faster in the oMP group (6.5 [3.00, 10.00] days vs. 8.00 [5.00, 11.00] days for imACTH and 8.00 [5.00, 13.00] days for oP, p = 0.025). Spasm control at 3, 6, and 12 months was also similar in the three groups (P = 0.775, 0.667, and 0.779). The relapse rate in the imACTH group (24.10%) was lower than oMP (30.77%) and oP groups (33.33%), and the time taken for relapse in the imACTH group (79.00 [56.50, 152.00] days) was longer than oMP (62.50 [38.00, 121.75] days) and oP groups (71.50 [40.00, 99.75] days), but the differences were not statistically significant (p = 0.539 and 0.530, respectively). The occurrence of adverse effects was similar among the three groups.
Conclusions: The short and intermediary-term efficacy and recurrence rates of oMP are not inferior to those of imACTH and oP for the treatment of IS. Significantly, the time to achieve electroclinical remission with oMP was quicker than that with imACTH and oP. Considering its convenience, affordability, and the absence of irreversible side effects, oMP can serve as a form of first-line treatment for newly diagnosed IS.

Adrenocorticotropic Hormone-Independent Cushing Syndrome with Right Adrenal Adenoma and HIV Infection: A Case Report

Background: Adrenocorticotropic hormone (ACTH)-independent Cushing’s syndrome (CS) with right adrenal adenoma combined with HIV infection has rarely been reported.
Case presentation: A 39-year-old Chinese male patient with HIV infection was admitted to our hospital due to increased blood pressure in the previous 2 years and weight gain in the previous 6 months. Endocrinological examinations showed that blood cortisol (8 a.m.) was 22.23 μg/dl, the level of ACTH (8 a.m.) was less than 1pg/ml and twenty-four-hour urinary cortisol was 1429 μg/24h. ACTH-independent CS was diagnosed based on low ACTH levels (<1.00 pg/ml), a lack of cortisol circadian rhythms, and unsuppressed cortisol levels by dexamethasone. The ultrasonography and multislice spiral computed tomography scan revealed a right adrenal mass. Due to the HIV status of the patient, we measured the count of CD4+ T helper cells. Laparoscopic right adrenal resection was performed after the CD4+ T helper cell count was > 200 cells/μl. Subsequent immunohistochemical staining confirmed right adrenal adenoma.
Results: The postoperative recovery was good, and wound healing was possible. After surgical treatment, endocrinological examinations indicated that the level of ACTH increased and the levels of serum cortisol and twenty-four-hour urinary cortisol decreased, which indicated that CS was controlled. CD4/CD8 was 0.47 at reexamination, and the patient’s immunity was improved.
Conclusion: Due to the potential side effects of steroid drugs, clinicians should use these medications with caution and closely monitor the development of adrenal deficiency.

Comparison of Bolus and Continuous Infusion of Adrenocorticotropic Hormone During Adrenal Vein Sampling

Background: Adrenocorticotropic hormone (ACTH) is widely used in adrenal vein sampling (AVS) and can be administered as a bolus injection or continuous infusion. The optimal administration method has not been determined. We aimed to compare the effects of ACTH bolus with infusion on cannulation success, lateralization assessment and adverse events (AEs).
Methods: Retrospectively collected data from patients with primary aldosteronism who underwent AVS with ACTH at a tertiary hospital in China. Rate of successful cannulation, lateralization index (LI), complete biochemical remission and AEs related to AVS were analyzed.
Results: The study included 80 patients receiving ACTH bolus and 94 receiving infusions. The rate of successful cannulation was comparable between bolus and infusion groups (75/80, 93.4% vs 88/94, 93.6%). In those with successful cannulation, the bolus group had a higher selectivity index than the infusion group, while LI [6.4(1.8-17.5) vs. 7.6(2.0-27.8), P=0.48] and rate of complete biochemical remission (43/44, 97.7% vs 53/53, 100%, P=0.45) did not significantly differ between the two groups. One in the bolus and one patient in the infusion group had adrenal vein rupture but they recovered with conservative treatment. The bolus group reported more transient AEs such as palpitation (52.9% vs 2.2%) and abdominal discomfort (40.0% vs 2.2%) than the infusion group.
Conclusions: Due to their similar effects on cannulation success and lateralization, but a lower rate of transient AEs in the infusion group, the continuous infusion method should be recommended for ACTH stimulation in AVS.

Cushing’s syndrome caused by intra-adrenocortical adrenocorticotropic hormone in a dog

A 13-year-old Labrador retriever was diagnosed with Cushing’s syndrome (CS) caused by primary bilateral nodular adrenocortical hyperplasia with adrenocorticotropic hormone (ACTH) expression. The pituitary origin of CS was ruled out by suppression of plasma ACTH concentration and absence of a proliferative lesion on histological evaluation of the pituitary gland using periodic acid-Schiff (PAS) staining, reticulin staining, and immunostaining for ACTH. A pheochromocytoma also was found at necropsy examination.
On histological evaluation of both adrenal glands, at the junction of the fascicular and glomerular zones, multiple cell clusters distributed in both hyperplastic adrenal cortices expressed ACTH, whereas the pheochromocytoma cells did not. These results indicate that a disease similar to primary bilateral macronodular adrenocortical hyperplasia in humans also occurs in dogs, with intra-adrenocortical expression of ACTH, glucocorticoids excess, and clinical signs of CS. Therefore, the term ACTH-independent could be inappropriate in some cases of bilateral adrenocortical hyperplasia and suppressed plasma ACTH concentration in dogs.

Adrenocorticotropic Hormone

7-02131 CHI Scientific 2mg Ask for price

Adrenocorticotropic Hormone

7-02132 CHI Scientific 10mg Ask for price

Adrenocorticotropic Hormone

7-02133 CHI Scientific 50mg Ask for price

ACTH (Adrenocorticotropic Hormone)

RA21005 Neuromics 50 ug 412.8 EUR

Adrenocorticotropic Hormone siRNA

20-abx929248 Abbexa
  • 661.20 EUR
  • 878.40 EUR
  • 15 nmol
  • 30 nmol

Adrenocorticotropic Hormone siRNA

20-abx929249 Abbexa
  • 661.20 EUR
  • 878.40 EUR
  • 15 nmol
  • 30 nmol

Human Adrenocorticotropic Hormone

RP-1503 Alpha Diagnostics 2 mg 196.8 EUR

Adrenocorticotropic Hormone Protein

20-abx262167 Abbexa
  • 393.60 EUR
  • 276.00 EUR
  • 910.80 EUR
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Adrenocorticotropic Hormone Protein

20-abx262825 Abbexa
  • 393.60 EUR
  • 7676.40 EUR
  • 276.00 EUR
  • 10 ug
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Adrenocorticotropic Hormone (34-39) Peptide

20-abx265802 Abbexa
  • 393.60 EUR
  • 594.00 EUR
  • 326.40 EUR
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Adrenocorticotropic Hormone (11-24) Peptide

20-abx266458 Abbexa
  • 661.20 EUR
  • 1111.20 EUR
  • 477.60 EUR
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Adrenocorticotropic Hormone (4-10) Peptide

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  • 427.20 EUR
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Adrenocorticotropic Hormone (1-10) Peptide

20-abx265057 Abbexa
  • 526.80 EUR
  • 861.60 EUR
  • 393.60 EUR
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Adrenocorticotropic Hormone (1-13) Peptide

20-abx265058 Abbexa
  • 627.60 EUR
  • 1045.20 EUR
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Adrenocorticotropic Hormone (5-10) Peptide

20-abx265808 Abbexa
  • 393.60 EUR
  • 594.00 EUR
  • 326.40 EUR
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Adrenocorticotropic Hormone (4-11) Peptide

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  • 460.80 EUR
  • 710.40 EUR
  • 360.00 EUR
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Adrenocorticotropic Hormone (1-14) Peptide

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  • 661.20 EUR
  • 1111.20 EUR
  • 477.60 EUR
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ACTH Adrenocorticotropic Hormone protein

PROTP01189-1 BosterBio Regular: 10mg 380.4 EUR

Adrenocorticotropic Hormone (ACTH) Antibody

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  • 493.20 EUR
  • 2214.00 EUR
  • 718.80 EUR
  • 218.40 EUR
  • 360.00 EUR
  • 100 ug
  • 1 mg
  • 200 ug
  • 20 ug
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Adrenocorticotropic Hormone (ACTH) Antibody

20-abx110468 Abbexa
  • 493.20 EUR
  • 2214.00 EUR
  • 718.80 EUR
  • 218.40 EUR
  • 360.00 EUR
  • 100 ug
  • 1 mg
  • 200 ug
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Adrenocorticotropic Hormone (ACTH) Antibody

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  • 477.60 EUR
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  • 1312.80 EUR
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Adrenocorticotropic Hormone (ACTH) Antibody

20-abx175279 Abbexa
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Adrenocorticotropic Hormone (ACTH) Antibody

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Adrenocorticotropic Hormone (ACTH) Antibody

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Adrenocorticotropic Hormone (ACTH) Antibody

abx430970-200ul Abbexa 200 ul 460.8 EUR

Exercise-induced adrenocorticotropic hormone response is cooperatively regulated by hypothalamic arginine vasopressin and corticotrophin-releasing hormone

Introduction: Exercise becomes a stress when performed at an intensity above the lactate threshold (LT) because at that point the plasma adrenocorticotropic hormone (ACTH), a marker of stress response, increases. It is possible that the exercise-induced ACTH response is regulated at least by arginine vasopressin (AVP) and possibly by corticotropin-releasing hormone (CRH), but this remains unclear. To clarify the involvement of these factors, it is useful to intervene pharmacologically in the regulatory mechanisms, with a physiologically acceptable exercise model.
Methods: We used a special stress model of treadmill running (aerobic exercise) for male Wistar rats, which mimic the human physiological response, where plasma ACTH levels increase at just above the LT for 30 min. Animals were administered the AVP V1b receptor antagonist SSR149415 (SSR) and/or the CRH type 1 receptor antagonist CP154526 (CP) intraperitoneally before the exercise, which allowed the monitoring of exercise-induced ACTH response. Immunocytochemical evaluation of activated AVP and CRH neurons with exercise was performed for the animals’ hypothalami.
Results: A single injection of either antagonist, SSR or CP, resulted in inhibited ACTH levels after exercise stress. Moreover, the combined injection of SSR and CP strongly suppressed ACTH secretion during treadmill running to a greater extent than each alone. The running-exercise-induced activation of both AVP and CRH neurons in the hypothalamus was also confirmed.
Conclusion: These results lead us to hypothesize that AVP and CRH are cooperatively involved in exercise-induced ACTH response just above the LT. This may also reflect the stress response with moderate-intensity exercise in humans.

A 4-hour Profile of 17-hydroxyprogesterone in Salt-wasting Congenital Adrenal Hyperplasia: Is the Serial Monitoring Strategy Worth the Effort?

Objective: Since there exists no gold standard laboratory variable for adjustment of treatment in congenital adrenal hyperplasia (CAH), we aimed to assess the use of a 4-hour profile of serum 17-OHP to determine the most appropriate time and level of 17-OHP in predicting the metabolic control and evaluate the role of sex hormone-binding globulin (SHBG) in hyperandrogenemia.
Methods: This study included 16 children (9 girls,7 boys; median age 7 years) with salt-wasting CAH. Measurements for 17-OHP and cortisol were made from samples obtained before and 1,2,4 hours after the morning dose of hydrocortisone. Patients were designated to have poor metabolic control when androstenedione levels according to age and sex-specific reference intervals were high and annual height SDS changes were ⩾0.5.
Results: Premedication 17-OHP levels were strongly correlated with 17-OHP levels 1, 2, 4 hours after the morning dose (rs=0.929, p<0.01; rs=0.943, p<0.01; rs=0.835, p<0.01, respectively). 17-OHP profiles (0,1,2,4 hours) of poor (n=6) and good (n=10) metabolically controlled cases were similar. Among the patients with poor metabolic control, two cases had 17-OHP levels <2 ng/mL at all times. Remaining patients with poor metabolic control had 17-OHP levels above 104 ng/mL, 82 ng/mL, 14 ng/mL, and 4 ng/mL, for baseline and 1, 2, and 4 hours, respectively. Differences between the poor and well-controlled group were androstenedione levels with respect to upper limit of normal [1.8(1.5) and 0.5(1.5) ng/mL, respectively p=0.03], annual change in height SDS [0.7(0.2) and -0.03(0.8) SDS, respectively, p=0.001], and daily hydrocortisone doses [7 (6) and 16 (8) mg/m2/day, respectively, p=0.02]. Androstenedione and SHBG levels were negatively correlated in the pubertal children (rs=-0.7, p=0.04).
Conclusion: We conclude that (i)a 4-hour 17-OHP profile is not useful in predicting hyperandrogenemia, (ii)suppressed levels of 17-OHP do not always indicate overtreatment, (iii)reference intervals of 17-OHP for different time periods might be of importance, (iv) low hydrocortisone doses should be avoided, (v)SHBG could be used in pubertal children as an indicator of hyperandrogenemia.

Eligibility, Utilization, and Effectiveness of 17-Alpha Hydroxyprogesterone Caproate (17OHPC) in a Statewide Population-Based Cohort of Medicaid Enrollees

Objectives: The primary objective was to estimate the initiation and adherence rates of 17 α-hydroxyprogesterone caproate (17OHPC) among eligible mothers in a statewide population-based cohort of Medicaid enrollees. The secondary objectives were to (1) determine the association of maternal sociodemographic and clinical characteristics with 17OHPC utilization and (2) assess the real-world effectiveness of 17OHPC on recurrent preterm birth prevention and admission to neonatal intensive care unit (NICU).
Study design: This is a retrospective cohort study using a linked, longitudinal administrative dataset of birth certificates and medical assistance claims. Medicaid-enrolled mothers in Pennsylvania were included in this study if they had at least one singleton live birth from 2014 to 2016 following at least one spontaneous preterm birth. Maternal Medicaid claims were used to ascertain the use of 17OHPC from various manufacturers, including compounded formulations. Propensity score matching was used to create a covariate balance between 17OHPC treatment and comparison groups.
Results: We identified 4,781 Medicaid-covered 17OHPC-eligible pregnancies from 2014 to 2016 in Pennsylvania, 3.4% of all Medicaid-covered singleton live births. The population-based initiation rate was 28.5% among eligible pregnancies. Among initiators, 50% received ≥16 doses as recommended, while 10% received a single dose only. The severity of previous spontaneous preterm birth was the strongest predictor for the initiation and adherence of 17OHPC. In the matched treatment (n = 1,210) and comparison groups (n = 1,210), we found no evidence of 17OHPC effectiveness. The risks of recurrent preterm birth (relative risk [RR] 1.10, 95% confidence interval [CI] 0.97-1.24) and births admitted to NICU (RR 1.00, 95% CI 0.84-1.18) were similar in treated and comparison mothers.
Conclusion: The 17OHPC-eligible population represented 3.4% of singleton live births. Less than one-third of eligible mothers initiated treatment. Among initiators, 50% were treatment adherent. We found no difference in the risk of recurrent preterm birth or admission to NICU between treatment and comparison groups.

A Possible Mechanism of Action of 17α-Hydroxyprogesterone Caproate: Enhanced IL-10 Production

Objective: The rate of recurrent spontaneous preterm birth (PTB) was reduced by 33% in the Maternal-Fetal Medicine Unit (MFMU) Network trial of 17α-hydroxyprogesterone caproate (17-OHPC), but the mechanism of action, 17 years later, remains elusive. The robustness of the interleukin-10 (IL-10) response to lipopolysaccharide (LPS) stimulation of leukocytes in pregnant women with a prior PTB correlates with gestational age at delivery. This study sought to determine if there is a relationship between the concentration of 17-OHPC and response to LPS stimulation.
Study design: We performed a secondary analysis of data from the Omega-3 MFMU trial which evaluated the effectiveness of omega-3 fatty acid supplementation in reducing recurrent PTB. We utilized previously characterized data from a subanalyses of the Omega-3 trial of IL-10 and tumor necrosis factor alpha (TNF-α) levels from peripheral blood mononuclear cells stimulated with LPS. Blood was obtained from enrolled women at 16 to 22 weeks’ gestation (baseline) and 25 to 28 weeks’ gestation (posttreatment). All women received 17-OHPC and plasma 17-OHPC concentrations were measured at 25 to 28 weeks’ gestation. We analyzed these data to determine if there was a relationship between 17-OHPC concentration and cytokine production. We then performed an in vitro study to determine if 17-OHPC could directly alter cytokine production by THP-1-derived macrophages.
Results: In the clinical samples, we found that 17-OHPC plasma concentrations were correlated with the quantity of the LPS-stimulated production of IL-10. TNF-α production after LPS stimulation was unrelated to 17-OHPC concentration. In the in vitro study, we demonstrate a 17-OHPC concentration dependent increase in IL-10 production.
Conclusion: In women receiving 17-OHPC for PTB prevention, we demonstrate a relationship between plasma 17-OHPC and LPS-stimulated IL-10 production by circulating leukocytes. We also demonstrate that, in vitro, 17-OHPC treatment affects IL-10 production by LPS-stimulated macrophages. Collectively, these findings support an immunomodulatory mechanism of action of 17-OHPC in the prevention of recurrent PTB.
Product not found

In utero exposure to 17α-hydroxyprogesterone caproate and risk of cancer in offspring

Background: 17α-hydroxyprogesterone caproate (17-OHPC) is a synthetic progestogen initially approved in the 1950s to treat gynecological and obstetrical conditions. Despite repeated concerns of safety and short-term efficacy regarding the use of 17-OHPC for the prevention of preterm birth in pregnant women, little is known about long-term effects of 17-OHPC on health of offspring.
Objective: To examine the association between in utero exposure to 17-OHPC and risk of cancer in offspring.
Study design: The Child Health and Development Studies is a population-based cohort of more than 18,000 mother-child dyads receiving prenatal care in the Kaiser Foundation Health Plan (Oakland, California) between 1959 and 1966. Clinical information was abstracted from mothers’ medical records beginning six months prior to pregnancy through delivery. We identified the number and timing of 17-OHPC injections during pregnancy. Incident cancers diagnosed in offspring were ascertained through 2019 by linkage to the California Cancer Registry. We used Cox proportional hazards models to estimate adjusted hazard ratios (aHR) and their 95% confidence intervals, with follow-up time accrued from date of birth through date of cancer diagnosis, death, or last contact.
Results: 1,008 offspring were diagnosed with cancer over 730,817 person-years of follow-up. About 1.0% of offspring (n=234) were exposed in utero to 17-OHPC. Exposure in the first trimester was associated with increased risk of any cancer (aHR 2.57, 95% CI 1.59, 4.15), and risk increased with number of injections (1-2 injections: aHR 1.80, 95% CI 1.12,2.90; ≥3 injections: aHR 3.07, 95% CI 1.34, 7.05). Exposure in the second or third trimester conferred an additional risk for male (aHR 2.59, 95% CI 1.07, 6.28) but not female (aHR 0.30, 0.04, 1.11) offspring. Risk of colorectal (aHR 5.51, 95% CI 1.73, 17.59), prostate (aHR 5.10, 95% CI 1.24, 21.00), and pediatric brain (aHR 34.72, 95% CI 7.29, 164.33) cancer was higher in offspring first exposed to 17-OHPC in the first trimester compared to offspring not exposed.

Clinical Response to Apatinib Combined With Brain Radiotherapy in EGFR Wild-Type and ALK-Negative Lung Adenocarcinoma With Multiple Brain Metastases.

Clinical Response to Apatinib Combined With Brain Radiotherapy in EGFR Wild-Type and ALK-Negative Lung Adenocarcinoma With Multiple Brain Metastases.

Background: Brain radiotherapy is the usual remedy possibility for a number of mind metastases (BMs) from non-small cell lung most cancers (NSCLC), particularly in the absence of a driver mutation. However, the prognosis for such sufferers stays poor. Apatinib is a potent antiangiogenic compound directed on the vascular endothelial progress issue receptor-2 (VEGFR-2); nevertheless, to date, there are not any investigations of apatinib concurrent with mind radiotherapy for NSCLC sufferers with BMs.

We report a case of EGFR wild-type and ALK-negative lung adenocarcinoma affected person with a number of symptomatic BMs, who obtained apatinib along with mind radiation remedy. A positive oncologic consequence was achieved for each mind metastatic lesions and the first pulmonary tumor. Case Presentation: A 61-year-old feminine (by no means smoker) who initially offered with headache and dizziness was recognized with lung adenocarcinoma with a number of mind metastasis (cT2aN3M1b stage IV), and was unfavorable for EGFR and ALK.

The affected person refused to obtain chemotherapy and was solely amenable to mind radiotherapy and focused remedy. After approval from the institutional ethics committee, she underwent concurrent oral apatinib (500 mg/day) with complete mind radiation remedy (WBRT) (37.5Gy) with simultaneous in-field increase (49.5Gy) in 15 fractions with picture guided intensity-modulated radiotherapy.

Three weeks later, neurologic signs totally ceased and a partial response (PR) for the BMs with near-complete decision of peritumoral mind edema was achieved. Chest CT carried out on the identical time and confirmed shrinkage of the lung main with a PR.

The affected person suffered grade III oral mucositis one week after mind radiotherapy and refused additional apatinib. At 12 months after mind radiotherapy, the mind tumors remained properly managed. Conclusions: This is the primary identified documentation of a speedy medical response of apatinib concurrent with mind radiotherapy in a lung adenocarcinoma affected person with symptomatic a number of BMs. Apatinib mixed with mind radiotherapy could possibly be another remedy possibility for BMs from NSCLC, particularly for these with no driver mutation. Further medical trials are required to corroborate this discovery.

Clinical Response to Apatinib Combined With Brain Radiotherapy in EGFR Wild-Type and ALK-Negative Lung Adenocarcinoma With Multiple Brain Metastases.
Clinical Response to Apatinib Combined With Brain Radiotherapy in EGFR Wild-Type and ALK-Negative Lung Adenocarcinoma With Multiple Brain Metastases.

Pattern of Pediatric Supracondylar Fracture Operated at A Rural Teaching Hospital of Nepal: A Descriptive Cross-sectional Study.

Supracondylar fracture of humerus is likely one of the frequent pediatric fractures encountered in our every day medical observe. The goal of this examine is to decide the sample of supracondylar fracture operated at rural educating hospital of Jumla, Karnali Nepal.A descriptive cross sectional examine was carried out at Jumla, Karnali after Institutional Review Committee approval.

Operating room notes from 15 May 2017 to 16 November 2019 had been retrieved to collect the next data: sufferers tackle, age, intercourse, aspect, harm mechanism, displacement, neurovascular harm, concurrent accidents, preliminary administration by conventional bone setters, time between harm and surgical procedure, operative method.

NOD2 antibody

70R-18913 Fitzgerald 50 ul 522 EUR
Description: Rabbit polyclonal NOD2 antibody

Nod2 antibody

10R-6553 Fitzgerald 100 ug 522 EUR
Description: Rat monoclonal Nod2 antibody

NOD2 Antibody

24158-100ul SAB 100ul 468 EUR

NOD2 Antibody

24159-100ul SAB 100ul 468 EUR

NOD2 Antibody

2511-002mg ProSci 0.02 mg 206.18 EUR
Description: NOD2 Antibody: Apaf-1 and NOD1 are members of a new family, which are involved in the regulation of apoptosis and immune response. Each of them contains a caspase recruitment domain (CARD) and a nucleotide-binding oligomerization domain (NOD). A third member in this family was recently identified and designated NOD2. NOD2 interacts with RICK via a homophilic CARD-CARD interaction. NOD2 activates NF-κB, which is regulated by its carboxy-terminal leucine-rich repeat domain that acts as an intracellular receptor for components of bacteria. The variants of NOD2, either a frameshift or a missense, were associated with Crohn's disease that is a main type of chronic inflammatory bowel disease.

NOD2 Antibody

2511-01mg ProSci 0.1 mg 523.7 EUR
Description: NOD2 Antibody: Apaf-1 and NOD1 are members of a new family, which are involved in the regulation of apoptosis and immune response. Each of them contains a caspase recruitment domain (CARD) and a nucleotide-binding oligomerization domain (NOD). A third member in this family was recently identified and designated NOD2. NOD2 interacts with RICK via a homophilic CARD-CARD interaction. NOD2 activates NF-κB, which is regulated by its carboxy-terminal leucine-rich repeat domain that acts as an intracellular receptor for components of bacteria. The variants of NOD2, either a frameshift or a missense, were associated with Crohn's disease that is a main type of chronic inflammatory bowel disease.

NOD2 Antibody

2513-002mg ProSci 0.02 mg 206.18 EUR
Description: NOD2 Antibody: Apaf-1 and NOD1 are members of a new family, which are involved in the regulation of apoptosis and immune response. Each of them contains a caspase recruitment domain (CARD) and a nucleotide-binding oligomerization domain (NOD). A third member in this family was recently identified and designated NOD2. NOD2 interacts with RICK via a homophilic CARD-CARD interaction. NOD2 activates NF-κB, which is regulated by its carboxy-terminal leucine-rich repeat domain that acts as an intracellular receptor for components of bacteria. The variants of NOD2, either a frameshift or a missense, were associated with Crohn's disease that is a main type of chronic inflammatory bowel disease.

NOD2 Antibody

2513-01mg ProSci 0.1 mg 523.7 EUR
Description: NOD2 Antibody: Apaf-1 and NOD1 are members of a new family, which are involved in the regulation of apoptosis and immune response. Each of them contains a caspase recruitment domain (CARD) and a nucleotide-binding oligomerization domain (NOD). A third member in this family was recently identified and designated NOD2. NOD2 interacts with RICK via a homophilic CARD-CARD interaction. NOD2 activates NF-κB, which is regulated by its carboxy-terminal leucine-rich repeat domain that acts as an intracellular receptor for components of bacteria. The variants of NOD2, either a frameshift or a missense, were associated with Crohn's disease that is a main type of chronic inflammatory bowel disease.

NOD2 Antibody

37460-100ul SAB 100ul 302.4 EUR

NOD2 Antibody

1-CSB-PA015915GA01HU Cusabio
  • 716.40 EUR
  • 399.60 EUR
  • 150ul
  • 50ul
Description: A polyclonal antibody against NOD2. Recognizes NOD2 from Human. This antibody is Unconjugated. Tested in the following application: ELISA, WB

NOD2 Antibody

1-CSB-PA876985 Cusabio
  • 380.40 EUR
  • 292.80 EUR
  • 100ul
  • 50ul
Description: A polyclonal antibody against NOD2. Recognizes NOD2 from Human. This antibody is Unconjugated. Tested in the following application: ELISA, IHC;ELISA:1:1000-1:2000, IHC:1:25-1:100

NOD2 Antibody

1-CSB-PA881021LA01HU Cusabio
  • 380.40 EUR
  • 402.00 EUR
  • 100ug
  • 50ug
Description: A polyclonal antibody against NOD2. Recognizes NOD2 from Human. This antibody is Unconjugated. Tested in the following application: ELISA, IHC, IF; Recommended dilution: IHC:1:20-1:200, IF:1:50-1:200

NOD2 Antibody

1-CSB-PA446192 Cusabio
  • 380.40 EUR
  • 292.80 EUR
  • 100ul
  • 50ul
Description: A polyclonal antibody against NOD2. Recognizes NOD2 from Human. This antibody is Unconjugated. Tested in the following application: ELISA, IHC;ELISA:1:2000-1:5000, IHC:1:50-1:200

NOD2 Antibody

DF12125 Affbiotech 200ul 420 EUR

NOD2 Antibody

R34436-100UG NSJ Bioreagents 100 ug 339.15 EUR
Description: Additional name(s) for this target protein: Nucleotide-binding oligomerization domain-containing protein 2, caspase recruitment domain family, member 15; CARD15

NOD2 Rabbit pAb

A15992-100ul Abclonal 100 ul 369.6 EUR

NOD2 Rabbit pAb

A15992-200ul Abclonal 200 ul 550.8 EUR

NOD2 Rabbit pAb

A15992-20ul Abclonal 20 ul 219.6 EUR

NOD2 Rabbit pAb

A15992-50ul Abclonal 50 ul 267.6 EUR

NOD2 Blocking Peptide

DF12125-BP Affbiotech 1mg 234 EUR

Polyclonal NOD2 Antibody

APR06297G Leading Biology 0.1 mg 790.8 EUR
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human NOD2 . This antibody is tested and proven to work in the following applications:

Polyclonal NOD2 Antibody

APR06298G Leading Biology 0.1 mg 790.8 EUR
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human NOD2 . This antibody is tested and proven to work in the following applications:

NOD2 Conjugated Antibody

C37460 SAB 100ul 476.4 EUR

Human NOD2 ELISA KIT

ELI-23582h Lifescience Market 96 Tests 988.8 EUR

Mouse Nod2 ELISA KIT

ELI-44123m Lifescience Market 96 Tests 1038 EUR

NOD2 ELISA KIT|Human

EF001273 Lifescience Market 96 Tests 826.8 EUR

Bovine NOD2 ELISA KIT

ELI-22273b Lifescience Market 96 Tests 1113.6 EUR

Human NOD2 shRNA Plasmid

20-abx961935 Abbexa
  • 961.20 EUR
  • 1345.20 EUR
  • 150 µg
  • 300 µg

TLR2 & NOD2-Based Adjuvant

VAdv-Ly0016 Creative Biolabs 5 mg 4016.4 EUR
Description: A TLR2 & NOD2-based vaccine adjuvant.

NOD2 Antibody, HRP conjugated

1-CSB-PA881021LB01HU Cusabio
  • 380.40 EUR
  • 402.00 EUR
  • 100ug
  • 50ug
Description: A polyclonal antibody against NOD2. Recognizes NOD2 from Human. This antibody is HRP conjugated. Tested in the following application: ELISA

NOD2 Antibody, FITC conjugated

1-CSB-PA881021LC01HU Cusabio
  • 380.40 EUR
  • 402.00 EUR
  • 100ug
  • 50ug
Description: A polyclonal antibody against NOD2. Recognizes NOD2 from Human. This antibody is FITC conjugated. Tested in the following application: ELISA

NOD2 Antibody, Biotin conjugated

1-CSB-PA881021LD01HU Cusabio
  • 380.40 EUR
  • 402.00 EUR
  • 100ug
  • 50ug
Description: A polyclonal antibody against NOD2. Recognizes NOD2 from Human. This antibody is Biotin conjugated. Tested in the following application: ELISA

Nod2 ORF Vector (Rat) (pORF)

ORF071395 ABM 1.0 ug DNA 607.2 EUR

NOD2 ORF Vector (Human) (pORF)

ORF026166 ABM 1.0 ug DNA 486 EUR

Nod2 ORF Vector (Mouse) (pORF)

ORF051499 ABM 1.0 ug DNA 607.2 EUR

NOD2 ELISA Kit (Human) (OKCD02031)

OKCD02031 Aviva Systems Biology 96 Wells 997.2 EUR
Description: Description of target: Involved in gastrointestinal immunity. Upon stimulation by muramyl dipeptide (MDP), a fragment of bacterial peptidoglycan, binds the proximal adapter receptor-interacting RIPK2, which recruits ubiquitin ligases as XIAP, BIRC2, BIRC3 and the LUBAC complex, triggering activation of MAP kinases and activation of NF-kappa-B signaling. This in turn leads to the transcriptional activation of hundreds of genes involved in immune response. Required for MDP-induced NLRP1-dependent CASP1 activation and IL1B release in macrophages.;Species reactivity: Human;Application: ;Assay info: Assay Methodology: Quantitative Sandwich Immunoassay;Sensitivity: < 0.055 ng/mL

NOD2 ELISA Kit (Mouse) (OKCA01740)

OKCA01740 Aviva Systems Biology 96 Wells 1015.2 EUR
Description: Description of target: Involved in gastrointestinal immunity. Upon stimulation by muramyl dipeptide (MDP), a fragment of bacterial peptidoglycan, binds the proximal adapter receptor-interacting RIPK2, which recruits ubiquitin ligases as XIAP, BIRC2, BIRC3 and the LUBAC complex, triggering activation of MAP kinases and activation of NF-kappa-B signaling. This in turn leads to the transcriptional activation of hundreds of genes involved in immune response (PubMed:22607974). Required for MDP-induced NLRP1-dependent CASP1 activation and IL1B release in macrophages (PubMed:18511561).;Species reactivity: Mouse;Application: ;Assay info: Assay Methodology: Quantitative Sanadwich ELISA;Sensitivity: 3.9 pg/mL

NOD2 ELISA Kit (Human) (OKCA02128)

OKCA02128 Aviva Systems Biology 96 Wells 999.6 EUR
Description: Description of target: Involved in gastrointestinal immunity. Upon stimulation by muramyl dipeptide (MDP), a fragment of bacterial peptidoglycan, binds the proximal adapter receptor-interacting RIPK2, which recruits ubiquitin ligases as XIAP, BIRC2, BIRC3 and the LUBAC complex, triggering activation of MAP kinases and activation of NF-kappa-B signaling. This in turn leads to the transcriptional activation of hundreds of genes involved in immune response. Required for MDP-induced NLRP1-dependent CASP1 activation and IL1B release in macrophages.;Species reactivity: Human;Application: ;Assay info: Assay Methodology: Quantitative Sandwich ELISA;Sensitivity: 6.25 pg/mL

NOD2 ELISA Kit (Human) (OKAN06319)

OKAN06319 Aviva Systems Biology 96 Wells 950.4 EUR
Description: Description of target: This gene is a member of the Nod1/Apaf-1 family and encodes a protein with two caspase recruitment (CARD) domains and six leucine-rich repeats (LRRs). The protein is primarily expressed in the peripheral blood leukocytes. It plays a role in the immune response to intracellular bacterial lipopolysaccharides (LPS) by recognizing the muramyl dipeptide (MDP) derived from them and activating the NFKB protein. Mutations in this gene have been associated with Crohn disease and Blau syndrome. Alternatively spliced transcript variants encoding distinct isoforms have been found for this gene.;Species reactivity: Human;Application: ELISA;Assay info: Assay Methodology: Quantitative Sandwich ELISA;Sensitivity: 0.055 ng/mL

Anti-CARD15 / NOD2 (Internal) antibody

STJ70992 St John's Laboratory 100 µg 430.8 EUR

h NOD2 inducible lentiviral particles

LVP627 GenTarget 1x107 IFU/ml x 200ul 541.2 EUR
Description: Pre-made over-expression lentivirus for expressing human target: NOD2 (nucleotide-binding oligomerization domain containing 2), [alternative names: ACUG; BLAU; CARD15; CD; CLR16.3; IBD1; NLRC2; NOD2B; PSORAS1]. The sub-cloned codon sequence is identical (100% match) to CDS region in NCBI ID: NM_022162.1. It also contains a RFP-Blasticidin dual selection marker.

Nod2 sgRNA CRISPR Lentivector set (Rat)

K6718501 ABM 3 x 1.0 ug 406.8 EUR

NOD2 3'UTR GFP Stable Cell Line

TU065801 ABM 1.0 ml 1636.8 EUR

Nod2 3'UTR GFP Stable Cell Line

TU264065 ABM 1.0 ml Ask for price

Nod2 3'UTR GFP Stable Cell Line

TU164191 ABM 1.0 ml Ask for price

Nod2 sgRNA CRISPR Lentivector set (Mouse)

K4411601 ABM 3 x 1.0 ug 406.8 EUR

NOD2 sgRNA CRISPR Lentivector set (Human)

K1438601 ABM 3 x 1.0 ug 406.8 EUR

NOD2 Protein Vector (Rat) (pPM-C-HA)

PV285580 ABM 500 ng 1399.2 EUR

NOD2 Protein Vector (Rat) (pPB-C-His)

PV285578 ABM 500 ng 1399.2 EUR

NOD2 Protein Vector (Rat) (pPB-N-His)

PV285579 ABM 500 ng 1399.2 EUR

NOD2 Protein Vector (Rat) (pPM-C-His)

PV285581 ABM 500 ng 1399.2 EUR

Polyclonal NOD2 / CARD15 Antibody (N-Terminus)

APR02524G Leading Biology 0.05mg 580.8 EUR
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human NOD2 / CARD15 (N-Terminus). This antibody is tested and proven to work in the following applications:

Polyclonal NOD2 / CARD15 Antibody (C-Terminus)

APR02525G Leading Biology 0.05mg 580.8 EUR
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human NOD2 / CARD15 (C-Terminus). This antibody is tested and proven to work in the following applications:

NOD2 Protein Vector (Mouse) (pPM-C-HA)

PV205996 ABM 500 ng 1278 EUR

NOD2 Protein Vector (Human) (pPM-C-HA)

PV104664 ABM 500 ng 973.2 EUR

NOD2 Protein Vector (Mouse) (pPB-C-His)

PV205994 ABM 500 ng 1278 EUR

NOD2 Protein Vector (Mouse) (pPB-N-His)

PV205995 ABM 500 ng 1278 EUR

NOD2 Protein Vector (Mouse) (pPM-C-His)

PV205997 ABM 500 ng 1278 EUR

NOD2 Protein Vector (Human) (pPB-C-His)

PV104662 ABM 500 ng 973.2 EUR

NOD2 Protein Vector (Human) (pPB-N-His)

PV104663 ABM 500 ng 973.2 EUR

NOD2 Protein Vector (Human) (pPM-C-His)

PV104665 ABM 500 ng 973.2 EUR

NOD2 3'UTR Luciferase Stable Cell Line

TU015801 ABM 1.0 ml 1636.8 EUR

Nod2 3'UTR Luciferase Stable Cell Line

TU114191 ABM 1.0 ml Ask for price

Nod2 3'UTR Luciferase Stable Cell Line

TU214065 ABM 1.0 ml Ask for price

Nod2 sgRNA CRISPR Lentivector (Rat) (Target 1)

K6718502 ABM 1.0 ug DNA 184.8 EUR

Nod2 sgRNA CRISPR Lentivector (Rat) (Target 2)

K6718503 ABM 1.0 ug DNA 184.8 EUR

Nod2 sgRNA CRISPR Lentivector (Rat) (Target 3)

K6718504 ABM 1.0 ug DNA 184.8 EUR

Nod2 sgRNA CRISPR Lentivector (Mouse) (Target 1)

K4411602 ABM 1.0 ug DNA 184.8 EUR

Nod2 sgRNA CRISPR Lentivector (Mouse) (Target 2)

K4411603 ABM 1.0 ug DNA 184.8 EUR

Nod2 sgRNA CRISPR Lentivector (Mouse) (Target 3)

K4411604 ABM 1.0 ug DNA 184.8 EUR

NOD2 sgRNA CRISPR Lentivector (Human) (Target 1)

K1438602 ABM 1.0 ug DNA 184.8 EUR

NOD2 sgRNA CRISPR Lentivector (Human) (Target 2)

K1438603 ABM 1.0 ug DNA 184.8 EUR

NOD2 sgRNA CRISPR Lentivector (Human) (Target 3)

K1438604 ABM 1.0 ug DNA 184.8 EUR

NOD2 Chemi-Luminescent ELISA Kit (Human) (OKCD03832)

OKCD03832 Aviva Systems Biology 96 Wells 1185.6 EUR
Description: Description of target: Involved in gastrointestinal immunity. Upon stimulation by muramyl dipeptide (MDP), a fragment of bacterial peptidoglycan, binds the proximal adapter receptor-interacting RIPK2, which recruits ubiquitin ligases as XIAP, BIRC2, BIRC3 and the LUBAC complex, triggering activation of MAP kinases and activation of NF-kappa-B signaling. This in turn leads to the transcriptional activation of hundreds of genes involved in immune response. Required for MDP-induced NLRP1-dependent CASP1 activation and IL1B release in macrophages .;Species reactivity: Human;Application: ;Assay info: Assay Methodology: Quantitative Sandwich ELISA;Sensitivity: 0.0412 ng/mL

Polyclonal Goat Anti-CARD15 / NOD2 (Internal) Antibody

APG00059G Leading Biology 0.1mg 580.8 EUR
Description: A polyclonal antibody raised in Goat that recognizes and binds to Human Goat Anti-CARD15 / NOD2 (Internal) . This antibody is tested and proven to work in the following applications:

NOD2 Lentiviral Vector (Rat) (CMV) (pLenti-GIII-CMV)

LV645601 ABM 1.0 ug DNA 1626 EUR

NOD2 Lentiviral Vector (Rat) (UbC) (pLenti-GIII-UbC)

LV645605 ABM 1.0 ug DNA 1626 EUR

NOD2 Lentiviral Vector (Rat) (EF1a) (pLenti-GIII-EF1a)

LV645606 ABM 1.0 ug DNA 1626 EUR

Nod2 sgRNA CRISPR/Cas9 All-in-One Lentivector set (Rat)

K6718505 ABM 3 x 1.0 ug 451.2 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody

abx235781-100ug Abbexa 100 ug 661.2 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody

20-abx114240 Abbexa
  • 878.40 EUR
  • 477.60 EUR
  • 150 ul
  • 50 ul

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody

20-abx302321 Abbexa
  • 493.20 EUR
  • 2214.00 EUR
  • 718.80 EUR
  • 218.40 EUR
  • 360.00 EUR
  • 100 ug
  • 1 mg
  • 200 ug
  • 20 ug
  • 50 ug

Nod2 sgRNA CRISPR/Cas9 All-in-One Lentivector set (Mouse)

K4411605 ABM 3 x 1.0 ug 451.2 EUR

NOD2 sgRNA CRISPR/Cas9 All-in-One Lentivector set (Human)

K1438605 ABM 3 x 1.0 ug 451.2 EUR

Nod2 sgRNA CRISPR/Cas9 All-in-One Lentivector (Rat) (Target 1)

K6718506 ABM 1.0 ug DNA 200.4 EUR

Nod2 sgRNA CRISPR/Cas9 All-in-One Lentivector (Rat) (Target 2)

K6718507 ABM 1.0 ug DNA 200.4 EUR

Nod2 sgRNA CRISPR/Cas9 All-in-One Lentivector (Rat) (Target 3)

K6718508 ABM 1.0 ug DNA 200.4 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody (HRP)

20-abx316579 Abbexa
  • 493.20 EUR
  • 2214.00 EUR
  • 718.80 EUR
  • 218.40 EUR
  • 360.00 EUR
  • 100 ug
  • 1 mg
  • 200 ug
  • 20 ug
  • 50 ug

Nod2 sgRNA CRISPR/Cas9 All-in-One Lentivector (Mouse) (Target 1)

K4411606 ABM 1.0 ug DNA 200.4 EUR

Nod2 sgRNA CRISPR/Cas9 All-in-One Lentivector (Mouse) (Target 2)

K4411607 ABM 1.0 ug DNA 200.4 EUR

Nod2 sgRNA CRISPR/Cas9 All-in-One Lentivector (Mouse) (Target 3)

K4411608 ABM 1.0 ug DNA 200.4 EUR

NOD2 sgRNA CRISPR/Cas9 All-in-One Lentivector (Human) (Target 1)

K1438606 ABM 1.0 ug DNA 200.4 EUR

NOD2 sgRNA CRISPR/Cas9 All-in-One Lentivector (Human) (Target 2)

K1438607 ABM 1.0 ug DNA 200.4 EUR

NOD2 sgRNA CRISPR/Cas9 All-in-One Lentivector (Human) (Target 3)

K1438608 ABM 1.0 ug DNA 200.4 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody (FITC)

20-abx316580 Abbexa
  • 493.20 EUR
  • 2214.00 EUR
  • 718.80 EUR
  • 218.40 EUR
  • 360.00 EUR
  • 100 ug
  • 1 mg
  • 200 ug
  • 20 ug
  • 50 ug

NOD2 Lentiviral Vector (Rat) (CMV) (pLenti-GIII-CMV-C-term-HA)

LV645602 ABM 1.0 ug DNA 1626 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody (Biotin)

20-abx316581 Abbexa
  • 493.20 EUR
  • 2214.00 EUR
  • 718.80 EUR
  • 218.40 EUR
  • 360.00 EUR
  • 100 ug
  • 1 mg
  • 200 ug
  • 20 ug
  • 50 ug

Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) Antibody

20-abx211027 Abbexa
  • 493.20 EUR
  • 360.00 EUR
  • 100 ul
  • 50 ul

Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) Antibody

20-abx339338 Abbexa
  • 493.20 EUR
  • 360.00 EUR
  • 100 ul
  • 50 ul

NOD2 Lentiviral Vector (Rat) (CMV) (pLenti-GIII-CMV-GFP-2A-Puro)

LV645603 ABM 1.0 ug DNA 1695.6 EUR

NOD2 Lentiviral Vector (Rat) (CMV) (pLenti-GIII-CMV-RFP-2A-Puro)

LV645604 ABM 1.0 ug DNA 1695.6 EUR

Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) CLIA Kit

20-abx190892 Abbexa
  • 9493.20 EUR
  • 5058.00 EUR
  • 1167.60 EUR
  • 10 × 96 tests
  • 5 × 96 tests
  • 96 tests

Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2)CLIA Kit

SCK295Hu-10x96wellstestplate Cloud-Clone 10x96-wells test plate 6777.36 EUR
Description: This is Double-antibody Sandwich Chemiluminescent immunoassay for detection of Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) in Tissue homogenates, cell lysates and other biological fluids.

Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2)CLIA Kit

SCK295Hu-1x48wellstestplate Cloud-Clone 1x48-wells test plate 663.31 EUR
Description: This is Double-antibody Sandwich Chemiluminescent immunoassay for detection of Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) in Tissue homogenates, cell lysates and other biological fluids.

Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2)CLIA Kit

SCK295Hu-1x96wellstestplate Cloud-Clone 1x96-wells test plate 896.16 EUR
Description: This is Double-antibody Sandwich Chemiluminescent immunoassay for detection of Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) in Tissue homogenates, cell lysates and other biological fluids.

Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2)CLIA Kit

SCK295Hu-5x96wellstestplate Cloud-Clone 5x96-wells test plate 3672.72 EUR
Description: This is Double-antibody Sandwich Chemiluminescent immunoassay for detection of Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) in Tissue homogenates, cell lysates and other biological fluids.

Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) CLIA Kit

4-SCK295Hu Cloud-Clone
  • 6837.60 EUR
  • 3673.20 EUR
  • 896.40 EUR
  • 10 plates of 96 wells
  • 5 plates of 96 wells
  • 1 plate of 96 wells
Description: Double-antibody Sandwich chemiluminescent immunoassay for detection of Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2)Tissue homogenates, cell lysates and other biological fluids

Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) ELISA Kit

20-abx258642 Abbexa
  • 8853.60 EUR
  • 4719.60 EUR
  • 1093.20 EUR
  • 10 × 96 tests
  • 5 × 96 tests
  • 96 tests

Human Nucleotide Binding Oligomerization Domain Containing Protein 2 ELISA Kit (NOD2)

RK01942 Abclonal 96 Tests 625.2 EUR

Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) ELISA Kit

SEK295Hu-10x96wellstestplate Cloud-Clone 10x96-wells test plate 5677.8 EUR
Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) in tissue homogenates, cell lysates and other biological fluids.

Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) ELISA Kit

SEK295Hu-1x48wellstestplate Cloud-Clone 1x48-wells test plate 572.76 EUR
Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) in tissue homogenates, cell lysates and other biological fluids.

Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) ELISA Kit

SEK295Hu-1x96wellstestplate Cloud-Clone 1x96-wells test plate 766.8 EUR
Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) in tissue homogenates, cell lysates and other biological fluids.

Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) ELISA Kit

SEK295Hu-5x96wellstestplate Cloud-Clone 5x96-wells test plate 3090.6 EUR
Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) in tissue homogenates, cell lysates and other biological fluids.

Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) ELISA Kit

4-SEK295Hu Cloud-Clone
  • 5738.40 EUR
  • 3031.20 EUR
  • 768.00 EUR
  • 10 plates of 96 wells
  • 5 plates of 96 wells
  • 1 plate of 96 wells
Description: Enzyme-linked immunosorbent assay based on the Double-antibody Sandwich method for detection of Human Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) in samples from tissue homogenates, cell lysates and other biological fluids with no significant corss-reactivity with analogues from other species.

Human Nucleotide-binding oligomerization domain-containing protein 2(NOD2) ELISA kit

CSB-EL015915HU-24T Cusabio 1 plate of 24 wells 198 EUR
Description: Quantitativesandwich ELISA kit for measuring Human Nucleotide-binding oligomerization domain-containing protein 2 (NOD2) in samples from serum, plasma, asciticfluid, tissue homogenates, cell lysates. A new trial version of the kit, which allows you to test the kit in your application at a reasonable price.

Human Nucleotide-binding oligomerization domain-containing protein 2(NOD2) ELISA kit

1-CSB-EL015915HU Cusabio
  • 964.80 EUR
  • 6118.80 EUR
  • 3244.80 EUR
  • 1 plate of 96 wells
  • 10 plates of 96 wells each
  • 5 plates of 96 wells each
Description: Quantitativesandwich ELISA kit for measuring Human Nucleotide-binding oligomerization domain-containing protein 2(NOD2) in samples from serum, plasma, asciticfluid, tissue homogenates, cell lysates. Now available in a cost efficient pack of 5 plates of 96 wells each, conveniently packed along with the other reagents in 5 separate kits.

ELISA kit for Human NOD2 (Nucleotide Binding Oligomerization Domain Containing Protein 2)

ELK5352 ELK Biotech 1 plate of 96 wells 518.4 EUR
Description: A sandwich ELISA kit for detection of Nucleotide Binding Oligomerization Domain Containing Protein 2 from Human in samples from blood, serum, plasma, cell culture fluid and other biological fluids.

Nod3l/ Rat Nod3l ELISA Kit

ELI-11062r Lifescience Market 96 Tests 1063.2 EUR

NOD1 siRNA

20-abx926109 Abbexa
  • 661.20 EUR
  • 878.40 EUR
  • 15 nmol
  • 30 nmol

NOD1 siRNA

20-abx926110 Abbexa
  • 661.20 EUR
  • 878.40 EUR
  • 15 nmol
  • 30 nmol

NOD1 Peptide

5947P ProSci 0.05 mg 197.7 EUR
Description: (CT) NOD1 peptide

NOD3 Peptide

5949P ProSci 0.05 mg 197.7 EUR
Description: (IN) NOD3 peptide

NOD4 Peptide

5951P ProSci 0.05 mg 197.7 EUR
Description: (NT) NOD4 peptide

NOD5 Peptide

5953P ProSci 0.05 mg 197.7 EUR
Description: (NT) NOD5 peptide

NOD6 Peptide

5955P ProSci 0.05 mg 197.7 EUR
Description: (NT) NOD6 peptide

NOD1 Rabbit pAb

A1246-100ul Abclonal 100 ul 369.6 EUR

NOD1 Rabbit pAb

A1246-200ul Abclonal 200 ul 550.8 EUR

NOD1 Rabbit pAb

A1246-20ul Abclonal 20 ul 219.6 EUR

NOD1 Rabbit pAb

A1246-50ul Abclonal 50 ul 267.6 EUR

NOD1 Peptide

42-460P ProSci 0.1 mg 405.6 EUR
Description: (CT) NOD1 Peptide

NOD1 Antibody

5947-002mg ProSci 0.02 mg 206.18 EUR
Description: NOD1 Antibody: NOD1 is a member of the NOD (nucleotide-binding oligomerization domain) family, a group of proteins that are involved in innate immune defense. NOD1 contains an N-terminal caspase recruitment domain (CARD), a centrally located nucleotide-binding domain (NBD), and ten tandem leucine-rich repeats (LRRs) in its C-terminus. The CARD is involved in apoptotic signaling, and NOD1 activates caspase-9 and NF-κB. LRRs participate in protein-protein interactions, and mutations in the NBD may affect the process of oligomerization and subsequent function of the LRR domain. This protein is an intracellular pattern-recognition receptor (PRR) that initiates inflammation in response to a subset of bacteria through the detection of bacterial diaminopimelic acid.

NOD1 Antibody

5947-01mg ProSci 0.1 mg 523.7 EUR
Description: NOD1 Antibody: NOD1 is a member of the NOD (nucleotide-binding oligomerization domain) family, a group of proteins that are involved in innate immune defense. NOD1 contains an N-terminal caspase recruitment domain (CARD), a centrally located nucleotide-binding domain (NBD), and ten tandem leucine-rich repeats (LRRs) in its C-terminus. The CARD is involved in apoptotic signaling, and NOD1 activates caspase-9 and NF-κB. LRRs participate in protein-protein interactions, and mutations in the NBD may affect the process of oligomerization and subsequent function of the LRR domain. This protein is an intracellular pattern-recognition receptor (PRR) that initiates inflammation in response to a subset of bacteria through the detection of bacterial diaminopimelic acid.

NOD3 Antibody

5949-002mg ProSci 0.02 mg 206.18 EUR
Description: NOD3 Antibody: NOD3 is a member of the NOD (nucleotide-binding oligomerization domain) family, a group of proteins that are involved in innate immune defense. NOD3 also known as NLR family CARD containing 3 (NLRC3), is predominantly expressed in the immune system, particularly in T lymphocytes, and its expression is strongly down-regulated following stimulation of the T-cell receptor complex and CD28, suggesting that NOD3 plays a role in attenuating the activation of T cells. NOD3 inhibits NF-kappaB, AP-1 and NFAT transcriptional activation in Jurkat T cells downstream of CD3/CD28 stimulation or treatment with PMA/ionomycin and decreases IL-2 and CD25 mRNA induction in activated cells.

NOD3 Antibody

5949-01mg ProSci 0.1 mg 523.7 EUR
Description: NOD3 Antibody: NOD3 is a member of the NOD (nucleotide-binding oligomerization domain) family, a group of proteins that are involved in innate immune defense. NOD3 also known as NLR family CARD containing 3 (NLRC3), is predominantly expressed in the immune system, particularly in T lymphocytes, and its expression is strongly down-regulated following stimulation of the T-cell receptor complex and CD28, suggesting that NOD3 plays a role in attenuating the activation of T cells. NOD3 inhibits NF-kappaB, AP-1 and NFAT transcriptional activation in Jurkat T cells downstream of CD3/CD28 stimulation or treatment with PMA/ionomycin and decreases IL-2 and CD25 mRNA induction in activated cells.

NOD4 Antibody

5951-002mg ProSci 0.02 mg 206.18 EUR
Description: NOD4 Antibody: NOD4 is a member of the NOD (nucleotide-binding oligomerization domain) family, a group of proteins that are involved in innate immune defense. NOD4 contains a CARD-like domain, a central NOD domain and a large LRR region. NOD4, an IFN-gamma-inducible nuclear protein, plays a role in homeostatic control of innate immunity and in antiviral defense mechanisms. As a key negative regulator of NF-κB and type I interferon signaling, NOD4 may be a useful target for manipulating immune responses against infectious or inflammation-associated diseases, including cancer.

NOD4 Antibody

5951-01mg ProSci 0.1 mg 523.7 EUR
Description: NOD4 Antibody: NOD4 is a member of the NOD (nucleotide-binding oligomerization domain) family, a group of proteins that are involved in innate immune defense. NOD4 contains a CARD-like domain, a central NOD domain and a large LRR region. NOD4, an IFN-gamma-inducible nuclear protein, plays a role in homeostatic control of innate immunity and in antiviral defense mechanisms. As a key negative regulator of NF-κB and type I interferon signaling, NOD4 may be a useful target for manipulating immune responses against infectious or inflammation-associated diseases, including cancer.

NOD5 Antibody

5953-002mg ProSci 0.02 mg 206.18 EUR
Description: NOD5 Antibody: NOD5, also known as NLRX1, is a member of the NOD (nucleotide-binding oligomerization domain) family, a group of proteins that are involved in innate immune defense. NOD5 localizes to the mitochondrial outer membrane and interacts with the virus-induced signaling adapter protein VISA. Unlike a subset of NOD-like receptors (NLRs) such as NOD1 and NOD2 which trigger pro-inflammatory cascades, and other NLRs that induce the caspase 1 inflammasome in response to immune challenges, NOD5 amplifies NF-κB and JNK pathways by inducing reactive oxygen species production.

NOD5 Antibody

5953-01mg ProSci 0.1 mg 523.7 EUR
Description: NOD5 Antibody: NOD5, also known as NLRX1, is a member of the NOD (nucleotide-binding oligomerization domain) family, a group of proteins that are involved in innate immune defense. NOD5 localizes to the mitochondrial outer membrane and interacts with the virus-induced signaling adapter protein VISA. Unlike a subset of NOD-like receptors (NLRs) such as NOD1 and NOD2 which trigger pro-inflammatory cascades, and other NLRs that induce the caspase 1 inflammasome in response to immune challenges, NOD5 amplifies NF-κB and JNK pathways by inducing reactive oxygen species production.

NOD6 Antibody

5955-002mg ProSci 0.02 mg 206.18 EUR
Description: NOD6 Antibody: NOD6, also known as NALP9, is a member of the NALP family, a group of proteins that typically contain a NACHT domain, a NACHT-associated domain (NAD), a C-terminal leucine-rich repeat (LRR) region, and an N-terminal pyrin domain (PYD) and are involved in inflammation and innate immune defense. The bovine NOD6, which has 76% homology to its human counterpart, has been suggested to be an oocyte marker gene. In adult tissues, NALP9 mRNA is expressed exclusively in ovary and testis.

NOD6 Antibody

5955-01mg ProSci 0.1 mg 523.7 EUR
Description: NOD6 Antibody: NOD6, also known as NALP9, is a member of the NALP family, a group of proteins that typically contain a NACHT domain, a NACHT-associated domain (NAD), a C-terminal leucine-rich repeat (LRR) region, and an N-terminal pyrin domain (PYD) and are involved in inflammation and innate immune defense. The bovine NOD6, which has 76% homology to its human counterpart, has been suggested to be an oocyte marker gene. In adult tissues, NALP9 mRNA is expressed exclusively in ovary and testis.

NOD1 antibody

70R-13231 Fitzgerald 100 ul 548.4 EUR
Description: Affinity purified Rabbit polyclonal NOD1 antibody

NOD1 Antibody

25174-100ul SAB 100ul 468 EUR

NOD3 Antibody

25175-100ul SAB 100ul 468 EUR

NOD4 Antibody

25176-100ul SAB 100ul 468 EUR

NOD5 Antibody

25177-100ul SAB 100ul 468 EUR

NOD6 Antibody

25178-100ul SAB 100ul 468 EUR

Nod1 antibody

22788-100ul SAB 100ul 468 EUR

NOD1 Antibody

ABD6378 Lifescience Market 100 ug 525.6 EUR

NOD1 Antibody

32256-100ul SAB 100ul 302.4 EUR

NOD1 Antibody

CSB-PA015914KA01HU- Cusabio each 402 EUR
Description: A polyclonal antibody against NOD1. Recognizes NOD1 from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: ELISA, WB, IHC;WB:1:500-1:2000, IHC:1:50-1:200

NOD1 Antibody

CSB-PA015914KA01HU-100ul Cusabio 100ul 466.8 EUR
Description: A polyclonal antibody against NOD1. Recognizes NOD1 from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: ELISA, WB, IHC;WB:1:500-1:2000, IHC:1:50-1:200

NOD1 Antibody

DF6378 Affbiotech 200ul 420 EUR

NOD1 Antibody

1-CSB-PA047815 Cusabio
  • 380.40 EUR
  • 292.80 EUR
  • 100ul
  • 50ul
Description: A polyclonal antibody against NOD1. Recognizes NOD1 from Human, Mouse. This antibody is Unconjugated. Tested in the following application: ELISA, IHC;ELISA:1:1000-1:5000, IHC:1:50-1:200

NOD1 Antibody

1-CSB-PA876477 Cusabio
  • 380.40 EUR
  • 292.80 EUR
  • 100ul
  • 50ul
Description: A polyclonal antibody against NOD1. Recognizes NOD1 from Human, Mouse. This antibody is Unconjugated. Tested in the following application: ELISA, IHC;ELISA:1:1000-1:5000, IHC:1:50-1:200

NOD1 Antibody

F54615-0.08ML NSJ Bioreagents 0.08 ml 140.25 EUR
Description: This gene encodes a member of the NOD (nucleotide-binding oligomerization domain) family. This member is a cytosolic protein. It contains an N-terminal caspase recruitment domain (CARD), a centrally located nucleotide-binding domain (NBD), and 10 tandem leucine-rich repeats (LRRs) in its C terminus. The CARD is involved in apoptotic signaling, LRRs participate in protein-protein interactions, and mutations in the NBD may affect the process of oligomerization and subsequent function of the LRR domain. This protein is an intracellular pattern-recognition receptor (PRR) that initiates inflammation in response to a subset of bacteria through the detection of bacterial diaminopimelic acid. Multiple alternatively spliced transcript variants differring in the 5' UTR have been described, but the full-length nature of these variants has not been determined.

NOD1 Antibody

F54615-0.4ML NSJ Bioreagents 0.4 ml 322.15 EUR
Description: This gene encodes a member of the NOD (nucleotide-binding oligomerization domain) family. This member is a cytosolic protein. It contains an N-terminal caspase recruitment domain (CARD), a centrally located nucleotide-binding domain (NBD), and 10 tandem leucine-rich repeats (LRRs) in its C terminus. The CARD is involved in apoptotic signaling, LRRs participate in protein-protein interactions, and mutations in the NBD may affect the process of oligomerization and subsequent function of the LRR domain. This protein is an intracellular pattern-recognition receptor (PRR) that initiates inflammation in response to a subset of bacteria through the detection of bacterial diaminopimelic acid. Multiple alternatively spliced transcript variants differring in the 5' UTR have been described, but the full-length nature of these variants has not been determined.

NOD1 Antibody

RQ5831 NSJ Bioreagents 100 ug 356.15 EUR
Description: Nucleotide-binding oligomerization domain-containing protein 1, also known as CARD4, is a protein receptor that in humans is encoded by the NOD1 gene. NOD1 is a member of NOD-like receptor protein family and is a close relative of NOD2. NOD1 is mapped to 7p14.3. It recognizes bacterial molecules and stimulates an immune reaction. NOD1 protein contains a caspase recruitment domain (CARD). This gene is an intracellular pattern recognition receptor, which is similar in structure to resistant proteins of plants, and mediates innate and acquired immunity by recognizing bacterial molecules containing D-glutamyl-meso-diaminopimelic acid (iE-DAP) moiety. What wore, it has been shown that NOD1 can sense cytosolic microbial products by monitoring the activation state of small Rho GTPases.

NOD1 Antibody

RQ6083 NSJ Bioreagents 100 ug 356.15 EUR
Description: Nucleotide-binding oligomerization domain-containing protein 1, also known as CARD4, is a protein receptor that in humans is encoded by the NOD1 gene. NOD1 is a member of NOD-like receptor protein family and is a close relative of NOD2. NOD1 is mapped to 7p14.3. It recognizes bacterial molecules and stimulates an immune reaction. NOD1 protein contains a caspase recruitment domain (CARD). This gene is an intracellular pattern recognition receptor, which is similar in structure to resistant proteins of plants, and mediates innate and acquired immunity by recognizing bacterial molecules containing D-glutamyl-meso-diaminopimelic acid (iE-DAP) moiety. What wore, it has been shown that NOD1 can sense cytosolic microbial products by monitoring the activation state of small Rho GTPases.

Nod1 Antibody

R31707 NSJ Bioreagents 100 ug 356.15 EUR
Description: Nucleotide-binding oligomerization domain-containing protein 1, also known as CARD4, is a protein receptor that in humans is encoded by the NOD1 gene. It is a member of NOD-like receptor protein family and is a close relative of Nod2. It recognizes bacterial molecules and stimulates an immune reaction. Nod1 contains a caspase recruitment domain (CARD). This gene is an intracellular pattern recognition receptor, which is similar in structure to resistant proteins of plants, and mediates innate and acquired immunity by recognizing bacterial molecules containing D-glutamyl-meso-diaminopimelic acid (iE-DAP) moiety. Additionally, it has been shown that Nod1 can sense cytosolic microbial products by monitoring the activation state of small Rho GTPases.

NOD1 Antibody

R33706-100UG NSJ Bioreagents 100 ug 339.15 EUR
Description: Additional name(s) for this target protein: Nucleotide-binding oligomerization domain containing 1

Mouse Nod1 ELISA KIT

ELI-35306m Lifescience Market 96 Tests 1038 EUR

Human NOD1 ELISA KIT

ELI-46124h Lifescience Market 96 Tests 988.8 EUR

NOD1 ELISA KIT|Human

EF005372 Lifescience Market 96 Tests 826.8 EUR

Nod1 ORF Vector (Rat) (pORF)

ORF071394 ABM 1.0 ug DNA 607.2 EUR

Mouse Nod1 Antibody

abx030859-400ul Abbexa 400 ul 627.6 EUR

Mouse Nod1 Antibody

abx030859-80l Abbexa 80 µl 343.2 EUR

NOD1 cloning plasmid

CSB-CL896866HU-10ug Cusabio 10ug 279.6 EUR
Description: A cloning plasmid for the NOD1 gene.

NOD1 ORF Vector (Human) (pORF)

ORF007140 ABM 1.0 ug DNA 114 EUR

Nod1 ORF Vector (Mouse) (pORF)

ORF051497 ABM 1.0 ug DNA 607.2 EUR

Nod1 ORF Vector (Mouse) (pORF)

ORF051498 ABM 1.0 ug DNA 607.2 EUR

NOD1 3'UTR GFP Stable Cell Line

TU065800 ABM 1.0 ml 1825.2 EUR

Nod1 3'UTR GFP Stable Cell Line

TU264064 ABM 1.0 ml Ask for price

Nod1 3'UTR GFP Stable Cell Line

TU164190 ABM 1.0 ml Ask for price

Human NOD1 shRNA Plasmid

20-abx957041 Abbexa
  • 961.20 EUR
  • 1345.20 EUR
  • 150 µg
  • 300 µg

Mouse NOD1 shRNA Plasmid

20-abx979820 Abbexa
  • 961.20 EUR
  • 1345.20 EUR
  • 150 µg
  • 300 µg

NOD1 Blocking Peptide

DF6378-BP Affbiotech 1mg 234 EUR

nod3l 3'UTR GFP Stable Cell Line

TU264066 ABM 1.0 ml Ask for price

Anti-NLRX1/Nod9 Antibody

A04980-1 BosterBio 100ul 476.4 EUR
Description: Rabbit Polyclonal Antibody for NLRX1 Antibody (NLRX1) detection.tested for IHC, WB in Human, Mouse, Rat.

Anti-CARD4/NOD1 Antibody

PB9294 BosterBio 100ug/vial 400.8 EUR

Anti-NLRX1 / NOD9 antibody

STJ72177 St John's Laboratory 100 µg 430.8 EUR

Polyclonal NOD1 Antibody

APR06661G Leading Biology 0.1 mg 790.8 EUR
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human NOD1 . This antibody is tested and proven to work in the following applications:

Polyclonal NOD3 Antibody

APR06662G Leading Biology 0.1 mg 790.8 EUR
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human NOD3 . This antibody is tested and proven to work in the following applications:

Polyclonal NOD4 Antibody

APR06663G Leading Biology 0.1 mg 790.8 EUR
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human NOD4 . This antibody is tested and proven to work in the following applications:

Polyclonal NOD5 Antibody

APR06664G Leading Biology 0.1 mg 790.8 EUR
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human NOD5 . This antibody is tested and proven to work in the following applications:

Polyclonal NOD6 Antibody

APR06665G Leading Biology 0.1 mg 790.8 EUR
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human NOD6 . This antibody is tested and proven to work in the following applications:

Polyclonal NOD1 Antibody

APR03070G Leading Biology 0.05ml 580.8 EUR
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human NOD1 . This antibody is tested and proven to work in the following applications:

NOD1 Conjugated Antibody

C32256 SAB 100ul 476.4 EUR

NOD1 ELISA Kit (Human) (OKEH08039)

OKEH08039 Aviva Systems Biology 96 Wells 1075.2 EUR
Description: Description of target: This gene encodes a member of the nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) family of proteins. The encoded protein plays a role in innate immunity by acting as a pattern-recognition receptor (PRR) that binds bacterial peptidoglycans and initiates inflammation. This protein has also been implicated in the immune response to viral and parasitic infection. Major structural features of this protein include an N-terminal caspase recruitment domain (CARD), a centrally located nucleotide-binding domain (NBD), and 10 tandem leucine-rich repeats (LRRs) in its C terminus. The CARD is involved in apoptotic signaling, LRRs participate in protein-protein interactions, and mutations in the NBD may affect the process of oligomerization and subsequent function of the LRR domain. Mutations in this gene are associated with asthma, inflammatory bowel disease, Behcet disease and sarcoidosis in human patients.;Species reactivity: Human;Application: ELISA;Assay info: Assay Methodology: Quantitative Sandwich ELISA;Sensitivity: 0.078 ng/mL

NOD1 ELISA Kit (Mouse) (OKEH08040)

OKEH08040 Aviva Systems Biology 96 Wells 1310.4 EUR
Description: Description of target: ;Species reactivity: Mouse;Application: ELISA;Assay info: Assay Methodology: Quantitative Competitive ELISA;Sensitivity: 0.096ng/mL

NOD1 ELISA Kit (Human) (OKCA00743)

OKCA00743 Aviva Systems Biology 96 Wells 999.6 EUR
Description: Description of target: Enhances caspase-9-mediated apoptosis. Induces NF-kappa-B activity via RIPK2 and IKK-gamma. Confers responsiveness to intracellular bacterial lipopolysaccharides (LPS). Forms an intracellular sensing system along with ARHGEF2 for the detection of microbial effectors during cell invasion by pathogens. Required for RHOA and RIPK2 dependent NF-kappa-B signaling pathway activation upon S.flexneri cell invasion. Involved not only in sensing peptidoglycan (PGN)-derived muropeptides but also in the activation of NF-kappa-B by Shigella effector proteins IpgB2 and OspB. Recruits NLRP10 to the cell membrane following bacterial infection.;Species reactivity: Human;Application: ;Assay info: Assay Methodology: Quantitative Sandwich ELISA;Sensitivity: 3.9 pg/mL

NOD1 Protein Vector (Rat) (pPM-C-HA)

PV285576 ABM 500 ng 1429.2 EUR

NOD1 Protein Vector (Rat) (pPB-C-His)

PV285574 ABM 500 ng 1429.2 EUR

NOD1 Protein Vector (Rat) (pPB-N-His)

PV285575 ABM 500 ng 1429.2 EUR

NOD1 Protein Vector (Rat) (pPM-C-His)

PV285577 ABM 500 ng 1429.2 EUR

NOD1 Protein Vector (Human) (pPM-C-HA)

PV028559 ABM 500 ng 394.8 EUR

NOD1 Protein Vector (Mouse) (pPM-C-HA)

PV205988 ABM 500 ng 1278 EUR

NOD1 Protein Vector (Mouse) (pPM-C-HA)

PV205992 ABM 500 ng 1278 EUR

Polyclonal NOD1 Antibody (C-term)

APR03618G Leading Biology 0.1ml 580.8 EUR
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human NOD1 (C-term). This antibody is tested and proven to work in the following applications:

NOD1 Protein Vector (Human) (pPB-C-His)

PV028557 ABM 500 ng 394.8 EUR

Data evaluation was performed utilizing Statistical Package for Social Sciences model 20.Left aspect predominated with 88 (63.7%) and extension kind was frequent in 135 (97.8%). Thirteen (9.4%) sufferers had been initially managed by conventional bonesetters. A complete of 138 kids underwent operative fixation with imply age of seven.47 years and gender ratio of two:1 boy to woman.

Fall from cliff, ladders and rooftops had been the prevailing explanation for harm 73 (52.8%). Average time between harm and surgical procedure was 5.2 days. Closed discount was performed in 100 (72.4%) sufferers whereas open discount was crucial in 38 (27.5%) sufferers.Closed extension kind pediatric supracondylar fracture was frequent in this examine. Fall from cliff, rooftop and ladder are the most important explanation for fracture. Delayed presentation and preliminary administration of the fracture by the standard bonesetters makes supracondylar fracture tougher in useful resource restricted setting like ours.