Mouse Adiponectin/Acrp30 ELISA Kit

Name: Mouse Adiponectin/Acrp30 ELISA Kit
SKU: DEIA2732
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

cell culture supernatants, tissues homogenates, serum, plasma

Species Reactivity

Mouse

Detection Method

Sandwich ELISA

Intended Use

For the quantitative determination of mouse Adiponectin concentrations in cell culture supernates, tissue homogenates, mouse serum, and plasma.

Contents of Kit

1. Mouse Adiponectin Microplates: 1 x 96 wells
2. Mouse Adiponectin Conjugate: 1 x 12.5 mL
3. Mouse Adiponectin Standard: 1 vial
4. Mouse Adiponectin Control: 1 vial
5. Assay Diluent: 1 x 12 mL
6. Calibrator Diluent Concentrate(4X): 2 x 21 mL
7. Wash Buffer Concentrate(25X): 1 x 50 mL
8. Color Reagent A: 1 x 12 mL
9. Color Reagent B: 1 x 12 mL
10. Stop Solution: 1 x 23 mL

Storage

Store at 2-8°C. Do not use past kit expiration date.

Precision

Intra-assay Precision: 5.8%-6.6%
Inter-assay Precision: 5.0%-6.4%

Detection Range

0.001-0.007 ng/mL

Sensitivity

0.003 ng/mL

Citations

Have you cited DEIA2732 in a publication? Let us know and earn a reward for your research.

Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Mendelian Randomization Analysis Identifies CpG Sites as Putative Mediators for Genetic Influences on Cardiovascular Disease Risk

AMERICAN JOURNAL OF HUMAN GENETICS

Authors: Richardson, Tom G.; Zheng, Jie; Smith, George Davey; Timpson, Nicholas J.; Gaunt, Tom R.; Relton, Caroline L.; Hemani, Gibran

Abstract

The extent to which genetic influences on cardiovascular disease risk are mediated by changes in DNA methylation levels has not been systematically explored. We developed an analytical framework that integrates genetic fine mapping and Mendelian randomization with epigenome-wide association studies to evaluate the causal relationships between methylation levels and 14 cardiovascular disease traits. We identified ten genetic loci known to influence proximal DNA methylation which were also associated with cardiovascular traits after multiple-testing correction. Bivariate fine mapping provided evidence that the individual variants responsible for the observed effects on cardiovascular traits at the ADCY3 and ADIPOQ loci were potentially mediated through changes in DNA methylation, although we highlight that we are unable to reliably separate causality from horizontal pleiotropy. Estimates of causal effects were replicated with results from large-scale consortia. Genetic variants and CpG sites identified in this study were enriched for histone mark peaks in relevant tissue types and gene promoter regions. Integrating our results with expression quantitative trait loci data, we provide evidence that variation at these regulatory regions is likely to also influence gene expression levels at these loci.

Genetic polymorphisms associated with overweight and obesity in uncontrolled Type 2 diabetes mellitus

BIOMARKERS IN MEDICINE

Authors: Kasim, Nor Bahirah; Huri, Hasniza Zaman; Vethakkan, Shireene Ratna; Ibrahim, Luqman; Abdullah, Bashar Mudhaffar

Abstract

Generally, obese and overweight individuals display higher free fatty acid levels, which stimulate insulin resistance. The combination of overweight or obesity with insulin resistance can trigger Type 2 diabetes mellitus (T2DM) and are primary contributing factors to the development of uncontrolled T2DM. Genetic polymorphisms also play an important role as they can impact a population's susceptibility to becoming overweight or obese and developing related chronic complications, such as uncontrolled T2DM. This review specifically examines the genetic polymorphisms associated with overweight and obesity in patients with uncontrolled T2DM. Particularly, gene polymorphisms in ADIPOQ (rs1501299 and rs17300539), LepR (rs1137101 and rs1045895), IRS2 (rs1805092), GRB14 (rs10195252 and rs3923113) and PPARG (rs1801282) have been associated with overweight and obesity in uncontrolled T2DM.