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Data show that JNK3 (zeige MAPK10 Proteine) silencing strongly decreases Insulin Receptor Substrate 2 (IRS2) protein expression.
IRS-1 (zeige IRS1 Proteine) and IRS-2 signaling interaction with the microtubule cytoskeleton and its response to AKT (zeige AKT1 Proteine) determines the response to microtubule disruption in breast carcinoma cells
The study results were suggestive of a positive association between Gly972Arg of IRS1 (zeige IRS1 Proteine) and PCOS in the south Indian population, while INS (zeige INS Proteine), IRS2, PPAR-G (zeige ARF6 Proteine) and CAPN10 (zeige CAPN10 Proteine) failed to show any association with PCOS in our studied population.
We concluded that USP15 (zeige USP15 Proteine) attenuates IGF-I (zeige IGF1 Proteine) signaling by antagonizing Nedd4 (zeige NEDD4 Proteine)-induced IRS-2 ubiquitination.
these data highlight two novel regulatory proteins that could be therapeutically manipulated to limit IL-4 (zeige IL4 Proteine)-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 (zeige IRS1 Proteine) 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 (zeige INSR Proteine) His 1058 C/T polymorphism may not be implicated in polycystic ovary syndrome.
In the renal proximal tubule, insulin (zeige INS Proteine) signaling via IRS1 (zeige IRS1 Proteine) is inhibited, while insulin (zeige INS Proteine) signaling via IRS2 is preserved. Insulin (zeige INS Proteine) 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 (zeige BRD2 Proteine) decreases IRS-2 mRNA degradation indicating post-transcriptional stabilization.
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 (zeige INS Proteine) sensing by NGNs and hyperphagic obese phenotype in IRS2 knockout mice
Mutation of five "inhibitory" Ser (zeige SIGLEC1 Proteine) 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 (zeige CAT Proteine) and superoxide dismutase (zeige SOD1 Proteine), and decreased nitric oxide synthase in 7- to 10-week-old IRS2(5A)-beta mice compared with IRS2(WT)-beta mice.
data identify SH2B1 (zeige SH2B1 Proteine) as a major regulator of IRS2 stability, demonstrate a novel feedback mechanism linking mTORC1 signaling with IRS2, and identify 4E-BP2 (zeige EIF4EBP2 Proteine) as a major regulator of proliferation and survival of beta-cells.
Decreased miR (zeige MLXIP Proteine)-33 levels can up-regulate IRS-2 expression, which appears to compensate for the defects of the insulin (zeige INS Proteine) signaling pathway in Irs-1 (zeige IRS1 Proteine) 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 (zeige DPP4 Proteine) inhibitor and PPARgamma (zeige PPARG Proteine) agonist exerts protective effects on pancreatic beta-cells in diabetic db/db (zeige LEPR Proteine) 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 (zeige INS Proteine) secretion.
The study identified the serine phosphorylation (p-Ser (zeige SIGLEC1 Proteine)) sites induced by PKC-Beta (zeige PRKCB Proteine) activation or AGT (zeige AGT Proteine), which inhibits insulin (zeige INS Proteine)-induced p-Tyr (zeige TYR Proteine) 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