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Data show that JNK3 (show MAPK10 Proteins) silencing strongly decreases Insulin Receptor Substrate 2 (IRS2) protein expression.
In the renal proximal tubule, insulin (show INS Proteins) signaling via IRS1 (show IRS1 Proteins) is inhibited, while insulin (show INS Proteins) signaling via IRS2 is preserved. Insulin (show INS Proteins) signaling via IRS2 continues to stimulate sodium reabsorption in the proximal tubule and causes sodium retention, edema, and hypertension.
miRNA-146a may function as a useful clinical tool in the treatment and diagnosis of ESCC, and its overexpression suppressed cell growth through inhibition of IRS2.
High IRS2 expression is associated with myeloproliferative neoplasms.
FSH (show BRD2 Proteins) decreases IRS-2 mRNA degradation indicating post-transcriptional stabilization.
These data demonstrate for the first time that miR146a suppresses lung cancer progression by repressing IRS2 expression
IRS (show IARS Proteins)-specific gene signatures represent accurate surrogates of IGF activity and could predict response to anti-IGF therapy in breast cancer.
Amplification of CUL4A (show CUL4A Proteins), IRS2, and TFDP1 (show TFDP1 Proteins) genes showed a significant difference in disease-free survival by both univariate and multivariate survival analyses in intrahepatic cholangiocarcinoma.
These results indicate that miR (show MLXIP Proteins)-106a* affects renal cell carcinoma (show MOK Proteins) (RCC (show XRCC1 Proteins)) progression by targeting IRS-2 with suppression of the PI3K (show PIK3CA Proteins)/Akt (show AKT1 Proteins) signaling pathway in RCC (show XRCC1 Proteins) cells
meta-analysis of genetic association studies: Data suggest that the D allele of the G1057D SNP in IRS2 has a significant effect on reducing risk of type 2 diabetes mellitus; obesity is a modifier of this association. [META-ANALYSIS, REVIEW]
We conclude that AFB1 may upregulate IRS2 and stimulate lung cancer cell migration through Src (show SRC Proteins)
Acute knockdown of Insr (show INSR Proteins) or both Irs1 (show IRS1 Proteins) and Irs2 in adipocytes increased Adipoq (show ADIPOQ Proteins) mRNA expression but reduced adiponectin (show ADIPOQ Proteins) secretion.
Combination of DPP-4 (show DPP4 Proteins) inhibitor and PPARgamma (show PPARG Proteins) agonist exerts protective effects on pancreatic beta-cells in diabetic db/db (show LEPR Proteins) mice through the augmentation of IRS-2 expression
discovered that Irs2 deficiency causes insulin resistance through up-regulation of the phosphatase and tensin homolog (PTEN). Importantly, suppressing PTEN in Irs2(-/-) podocytes rescued insulin sensitivity
A knockout mouse has confirmed the importance of IRS2 in the control of glucose homeostasis and especially in the survival and function of pancreatic beta-cells.
The data suggest that Irs2 deletion in endothelial cells leads to a decreased islet blood flow, which may cause impaired glucose-induced insulin (show INS Proteins) secretion.
Results indicate that although IRS (show IARS Proteins) isoforms (irs1 (show IRS1 Proteins) and irs2) play divergent roles in the developmental regulation of cardiac size, these isoforms exhibit nonredundant roles in mediating the hypertrophic and metabolic response of the heart to exercise.
Inhibition of Gsk-3beta by Irs-2-dependent PI3K signaling promotes glucose uptake and aerobic glycolysis.
Data (including data from knockout mice) suggest that Irs2 is not required for islet beta-cell proliferation (as seen with high-fat diet) but may be needed for beta-cell regeneration (as seen after partial pancreatectomy).
IRS2 plays a critical role in testicular development, potentially by mediating IGF1 (show IGF1 Proteins) signaling during embryonic and early postnatal development.
Mice with combined cardiomyocyte-specific deletion of Irs1 & Irs2 (show IRS1 Proteins) had unrestrained autophagy in cardiomyocytes, leading to myocyte loss, heart failure, premature death, apoptosis & mitochondrial dysfunction.
The study identified the serine phosphorylation (p-Ser (show SIGLEC1 Proteins)) sites induced by PKC-Beta (show PRKCB Proteins) activation or AGT (show AGT Proteins), which inhibits insulin (show INS Proteins)-induced p-Tyr (show TYR Proteins) sites on IRS2 and its signals in endothelial cells.
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.
insulin receptor substrate 2
, tyrosine kinase substrate