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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 (show MAPK10 ELISA Kits) silencing strongly decreases Insulin Receptor Substrate 2 (IRS2) protein expression.
IRS-1 (show IRS1 ELISA Kits) and IRS-2 signaling interaction with the microtubule cytoskeleton and its response to AKT (show AKT1 ELISA Kits) determines the response to microtubule disruption in breast carcinoma cells
The study results were suggestive of a positive association between Gly972Arg of IRS1 (show IRS1 ELISA Kits) and PCOS in the south Indian population, while INS (show INS ELISA Kits), IRS2, PPAR-G (show ARF6 ELISA Kits) and CAPN10 (show CAPN10 ELISA Kits) failed to show any association with PCOS in our studied population.
We concluded that USP15 (show USP15 ELISA Kits) attenuates IGF-I (show IGF1 ELISA Kits) signaling by antagonizing Nedd4 (show NEDD4 ELISA Kits)-induced IRS-2 ubiquitination.
these data highlight two novel regulatory proteins that could be therapeutically manipulated to limit IL-4 (show IL4 ELISA Kits)-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 (show IRS1 ELISA Kits) 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 (show INSR ELISA Kits) His 1058 C/T polymorphism may not be implicated in polycystic ovary syndrome.
In the renal proximal tubule, insulin (show INS ELISA Kits) signaling via IRS1 (show IRS1 ELISA Kits) is inhibited, while insulin (show INS ELISA Kits) signaling via IRS2 is preserved. Insulin (show INS ELISA Kits) 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 ELISA Kits) decreases IRS-2 mRNA degradation indicating post-transcriptional stabilization.
possible link between impaired insulin (show INS ELISA Kits) sensing by NGNs and hyperphagic obese phenotype in IRS2 knockout mice
Mutation of five "inhibitory" Ser (show SIGLEC1 ELISA Kits) 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 (show CAT ELISA Kits) and superoxide dismutase (show SOD1 ELISA Kits), and decreased nitric oxide synthase (show NOS ELISA Kits) in 7- to 10-week-old IRS2(5A)-beta mice compared with IRS2(WT)-beta mice.
data identify SH2B1 (show SH2B1 ELISA Kits) as a major regulator of IRS2 stability, demonstrate a novel feedback mechanism linking mTORC1 signaling with IRS2, and identify 4E-BP2 (show EIF4EBP2 ELISA Kits) as a major regulator of proliferation and survival of beta-cells.
Decreased miR (show MLXIP ELISA Kits)-33 levels can up-regulate IRS-2 expression, which appears to compensate for the defects of the insulin (show INS ELISA Kits) signaling pathway in Irs-1 (show IRS1 ELISA Kits) 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 (show DPP4 ELISA Kits) inhibitor and PPARgamma (show PPARG ELISA Kits) agonist exerts protective effects on pancreatic beta-cells in diabetic db/db (show LEPR ELISA Kits) 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 ELISA Kits) secretion.
Results indicate that although IRS (show IARS ELISA Kits) isoforms (irs1 (show IRS1 ELISA Kits) 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.
The study identified the serine phosphorylation (p-Ser (show SIGLEC1 ELISA Kits)) sites induced by PKC-Beta (show PRKCB ELISA Kits) activation or AGT (show AGT ELISA Kits), which inhibits insulin (show INS ELISA Kits)-induced p-Tyr (show TYR ELISA Kits) 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