Use your antibodies-online credentials, if available.
Select your species
Rat (Rattus) IRS2 ELISA Kit for Sandwich ELISA - ABIN434009
Głombik, Ślusarczyk, Trojan, Chamera, Budziszewska, Lasoń, Basta-Kaim: Regulation of insulin receptor phosphorylation in the brains of prenatally stressed rats: New insight into the benefits of antidepressant drug treatment. in European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology 2017
Data show that JNK3 (显示 MAPK10 ELISA试剂盒) silencing strongly decreases Insulin Receptor Substrate 2 (IRS2) protein expression.
IRS-1 (显示 IRS1 ELISA试剂盒) and IRS-2 signaling interaction with the microtubule cytoskeleton and its response to AKT (显示 AKT1 ELISA试剂盒) determines the response to microtubule disruption in breast carcinoma cells
The study results were suggestive of a positive association between Gly972Arg of IRS1 (显示 IRS1 ELISA试剂盒) and PCOS in the south Indian population, while INS (显示 INS ELISA试剂盒), IRS2, PPAR-G (显示 ARF6 ELISA试剂盒) and CAPN10 (显示 CAPN10 ELISA试剂盒) failed to show any association with PCOS in our studied population.
We concluded that USP15 (显示 USP15 ELISA试剂盒) attenuates IGF-I (显示 IGF1 ELISA试剂盒) signaling by antagonizing Nedd4 (显示 NEDD4 ELISA试剂盒)-induced IRS-2 ubiquitination.
these data highlight two novel regulatory proteins that could be therapeutically manipulated to limit IL-4 (显示 IL4 ELISA试剂盒)-induced IRS-2 signaling and polarization of M2 macrophages in allergic inflammation.
Proteasomal inhibition prolonged IRS-2 tyrosine phosphorylation, increased ubiquitination of IRS-2, and enhanced M2 gene expression.
Findings suggest that insulin receptor substrate -1 (显示 IRS1 ELISA试剂盒) Gly972Arg polymorphism is associated with polycystic ovary syndrome in the Caucasian ethnicity, and insulin receptor substrate -2 Gly1057Asp polymorphism is correlated with polycystic ovary syndrome in the Asian ethnicity. However, insulin receptor (显示 INSR ELISA试剂盒) His 1058 C/T polymorphism may not be implicated in polycystic ovary syndrome.
In the renal proximal tubule, insulin (显示 INS ELISA试剂盒) signaling via IRS1 (显示 IRS1 ELISA试剂盒) is inhibited, while insulin (显示 INS ELISA试剂盒) signaling via IRS2 is preserved. Insulin (显示 INS ELISA试剂盒) 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 (显示 BRD2 ELISA试剂盒) decreases IRS-2 mRNA degradation indicating post-transcriptional stabilization.
diabetes in IRS2-deficient male mice is associated with increased oxidative stress and apoptosis in the hypothalamus.
identified a critical inhibitory loop downstream of IRS2, demonstrating an unanticipated and previously unrecognized role for IRS2 in suppressing allergic lung inflammation and remodeling.
possible link between impaired insulin (显示 INS ELISA试剂盒) sensing by NGNs and hyperphagic obese phenotype in IRS2 knockout mice
Mutation of five "inhibitory" Ser (显示 SIGLEC1 ELISA试剂盒) phosphorylation sites on IRS2 in transgenic mice that overexpress, selectively in pancreatic beta-cells, either wild-type (WT) or a mutated IRS2 protein (IRS2(5A)) led to increased islets size, number, and mRNA levels of catalase (显示 CAT ELISA试剂盒) and superoxide dismutase (显示 SOD1 ELISA试剂盒), and decreased nitric oxide synthase (显示 NOS ELISA试剂盒) in 7- to 10-week-old IRS2(5A)-beta mice compared with IRS2(WT)-beta mice.
data identify SH2B1 (显示 SH2B1 ELISA试剂盒) as a major regulator of IRS2 stability, demonstrate a novel feedback mechanism linking mTORC1 signaling with IRS2, and identify 4E-BP2 (显示 EIF4EBP2 ELISA试剂盒) as a major regulator of proliferation and survival of beta-cells.
Decreased miR (显示 MLXIP ELISA试剂盒)-33 levels can up-regulate IRS-2 expression, which appears to compensate for the defects of the insulin (显示 INS ELISA试剂盒) signaling pathway in Irs-1 (显示 IRS1 ELISA试剂盒) deficient mice.
Acute knockdown of Insr or both Irs1 and Irs2 in adipocytes increased Adipoq mRNA expression but reduced adiponectin secretion.
Combination of DPP-4 (显示 DPP4 ELISA试剂盒) inhibitor and PPARgamma (显示 PPARG ELISA试剂盒) agonist exerts protective effects on pancreatic beta-cells in diabetic db/db (显示 LEPR ELISA试剂盒) 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 study identified the serine phosphorylation (p-Ser (显示 SIGLEC1 ELISA试剂盒)) sites induced by PKC-Beta (显示 PRKCB ELISA试剂盒) activation or AGT (显示 AGT ELISA试剂盒), which inhibits insulin (显示 INS ELISA试剂盒)-induced p-Tyr (显示 TYR ELISA试剂盒) 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