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Validated All-in-One™ qPCR Primer for IRS2(NM_003749.3) Search again
Product ID:
HQP164440
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
IRS-2
Gene Description:
insulin receptor substrate 2
Target Gene Accession:
NM_003749.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene encodes the insulin receptor substrate 2, a cytoplasmic signaling molecule that mediates effects of insulin, insulin-like growth factor 1, and other cytokines by acting as a molecular adaptor between diverse receptor tyrosine kinases and downstream effectors. The product of this gene is phosphorylated by the insulin receptor tyrosine kinase upon receptor stimulation, as well as by an interleukin 4 receptor-associated kinase in response to IL4 treatment. [provided by RefSeq].
Gene References into function
- IRS-2, not IRS-1, signals insulin activation of glycogen synthase in the L6hIR skeletal muscle cells. In these cells, insulin inhibition of GSK3 alpha and -beta requires dual phosphorylation by both Akt/PKB and PKC zeta.
- the 5' flanking sequence of IRS2 was investigated and two single nucleotide polymorphisms (SNPs) were identified; the SNP at -765 was suggested to be involved in the insulin-mediated regulation of the transcriptional activity of IRS2
- Relationship of genotypes to phenotypic features of polycystic ovary syndrome
- Data suggest that insulin receptor substrate-2 (IRS-2) is needed to maintain the predominance of bone formation over bone resorption, whereas IRS-1 maintains bone turnover.
- inhibition of insulin-stimulated insulin receptor substrate (IRS)-phosphatidylinositol 3-kinase/Akt signaling pathway by disrupting the association of IRS-1/IRS-2 with the insulin receptor
- Polymorphisms of the insulin receptor substrate-2 in patients with type 2 diabetes. No major role of IRS-2 polymorphisms in the pathogenesis of type 2 diabetes.
- Mutations in IRS2 gene are associated with severe obesity
- the association of homozygosity for the Asp1057 allele in IRS-2 with type 2 diabetes in Pima Indians may be mediated by interaction of the polymorphism with obesity on several diabetes-related traits
- IRS-2 is degraded by estrogen receptor alpha and is not involved in IGF-I signaling
- Progesterone crosstalks with insulin-like growth factor signaling in breast cancer cells via induction of IRS2.
- Both of the IRS proteins modulate VPF/VEGF expression in pancreatic cancer cells by different mechanistic pathways.
- B cells derived from transgenic mice expressing IRS2 levels elevated by 2- to 3-fold demonstrate alterations in the B cell intrinsic density-dependence of IgE and IgG1 production in vitro and an elevated serum IgE response after in vivo challenge.
- IRS-2-dependent IL-4 signaling in macrophages is impaired in models of type 2 diabetes mellitus through a mechanism that relies on insulin/glucose-dependent Ser/Thr-Pro motif serine phosphorylation mediated by the mTOR pathway
- data demonstrate cell-specific alterations in IRS protein concentrations in theca cells from polycystic ovaries consistent with exaggerated amplification of the insulin signal & which may play a role in ovarian hyperandrogenism & thecal hyperplasia
- The IRS2 G972R heterozygote GD genotype significantly reduced risk of colon cancer (odds ratio 0.8, 95% CI 0.6-0.9)except for those with the IRS1 R allele.
- IRS-2/PI 3-kinase pathway does not restore insulin-stimulated glucose uptake in myotubes from Type 2 diabetic patients.
- SH2-B dramatically enhanced leptin-stimulated tyrosine phosphorylation of IRS1 and IRS2 in human and mouse cells.
- type 2 diabetic patients, particularly obese patients, carrying the D1057 allele and the CA haplotype were associated with insulin resistance
- Carriers of Pro allele compared with carriers of Ala allele of PPARG2 gene had higher frequency of insulin resistance. No association was found between insulin resistance and alleles and genotypes of PPAR and IRS2 genes.
- Data show that the relationships between G1057D variants of IRS2 and type 2 diabetes mellitus are mediated by obesity.
- Emergence of IRS-2 overexpression at preneoplastic stages during experimental hepatocarcinogenesis and its protective effect against apoptosis suggest that IRS-2 contributes to liver tumor progression.
- IRS-1 and -2 degradation are mediated by phosphatidylinositol 3-kinase and proteasome sensitive pathway. High levels of IGF-IR, and possibly the subsequent increase in Akt phosphorylation, are required for efficient IRS degradation.
- after an acute bout of exercise, insulin-stimulated IRS-2 signaling is enhanced in human skeletal muscle
- Transgenic mice overexpressing IRS2 in the mammary gland show progressive mammary hyperplasia, tumorigenesis and metastasis.
- Genetic variation in IRS2 is associated with breast cancer risk
- phosphorylation is a mechanism for regulation of insulin receptor substrate-1/2, Akt, and ERK1/2
- We showed that clearance of HCV improves insulin resistance, beta-cell function, and hepatic IRS1/2 expression.
- This review points out that IRS-2, which is implicated in mediating signals to promote tumor cell survival, growth and motility, is a positive regulator of breast cancer metastasis.
- This review discusses the roles of IRS-1 and IRS-2 in oncogenic transformation and cancer progression.
- possible regulatory effect of SirT1 on insulin-induced tyrosine phosphorylation of IRS-2, a vital step in insulin signaling pathway, through deacetylation of IRS-2 protein.
- Altered osteoblast proliferation in human osteoporosis may result from dysregulation of IGF-I receptor signaling, including constitutive activation of the IRS-2/Erk signaling pathway.
- IRS2 expression was localised to macrophages and endothelial cells in vivo. The elevated IRS2 gene expression in macrophages may be associated with an increased risk of CHD.
- contribution of defective Irs2 signaling to metabolic syndrome-associated alterations
- IL-4 induced highly efficient, gammaC-dependent tyrosine phosphorylation of IRS-2, whereas IL-13 was less effective, even when phosphorylation of STAT6 was maximal
- Regulatory role of IRS-2 on the expression of IGF-I receptor through Protein kinase c-delta in pancreatic cancer cells.