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anti-Human IRS2 Antikörper:
anti-Rat (Rattus) IRS2 Antikörper:
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Human Monoclonal IRS2 Primary Antibody für ELISA, WB - ABIN534395
White: IRS proteins and the common path to diabetes. in American journal of physiology. Endocrinology and metabolism 2002
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Human Polyclonal IRS2 Primary Antibody für IF (p), IHC (p) - ABIN725840
Ling, Xie, Li, Liu, Cao, Yang, Wang, Hu, Xu, Zheng: Donor Graft MicroRNAs: A Newly Identified Player in the Development of New-onset Diabetes After Liver Transplantation. in American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons 2016
Show all 2 Pubmed References
Polyclonal IRS2 Primary Antibody für DB, IHC (fro) - ABIN541009
Li, Soos, Li, Wu, Degennaro, Sun, Littman, Birnbaum, Polakiewicz: Protein kinase C Theta inhibits insulin signaling by phosphorylating IRS1 at Ser(1101). in The Journal of biological chemistry 2004
Data show that JNK3 silencing strongly decreases Insulin Receptor Substrate 2 (IRS2) protein expression.
These findings indicated that the 3'UTR of IRS2 may be directly targeted by miR766 in papillary thyroid cancer (PTC) cells. Its knockdown simulates tumor suppressor activity of miR766 in PTC cells and its reintroduction of IRS2 rescues the effects of miR766 on the malignant behaviors of PTC cells.
miR-431 inhibits adipogenic differentiation of human mesenchymal stem cells via targeting IRS2.
Study suggests that polymorphisms of IRS2 putatively participated in the development of pediatric MB development.
Urinary sediment cell expression of IRS2 gene was significantly increased in the diabetic nephropathy (DN) patients compared with other groups. In patients with DN, urinary mRNA expression of the IRS2 gene is associated with kidney function.
Insulin signaling pathway protects neuronal cell lines by Sirt3 mediated IRS2 activation.
Acute loss of IRS1/IRS2 or inhibition of IR/IGF1R in KRAS-mutant human NSCLC cells decreases the uptake and lowers the intracellular levels of amino acids, while enhancing basal autophagy and sensitivity to autophagy and proteasome inhibitors.
that MTNR1B and IRS2 gene variants impacted epicardial fat thickness, lipid profile and glucose homeostasis
this meta-analysis indicates that IRS-2 gene rs1805097 polymorphism decreased the risk of CRC.
IRS-1 and IRS-2 signaling interaction with the microtubule cytoskeleton and its response to AKT determines the response to microtubule disruption in breast carcinoma cells
The study results were suggestive of a positive association between Gly972Arg of IRS1 and PCOS in the south Indian population, while INS, IRS2, PPAR-G and CAPN10 failed to show any association with PCOS in our studied population.
We concluded that USP15 attenuates IGF-I signaling by antagonizing Nedd4-induced IRS-2 ubiquitination.
these data highlight two novel regulatory proteins that could be therapeutically manipulated to limit IL-4-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 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 His 1058 C/T polymorphism may not be implicated in polycystic ovary syndrome.
In the renal proximal tubule, insulin signaling via IRS1 is inhibited, while insulin signaling via IRS2 is preserved. Insulin 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 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-specific gene signatures represent accurate surrogates of IGF activity and could predict response to anti-IGF therapy in breast cancer.
IRS2 plays an important role in the regulation of cell proliferation and steroidogenesis in mouse granulosa cells via the PI3K/AKT signaling pathway
Data (including data from studies using knockout mice) suggest that Irs2 is required to prevent insulin resistance as seen in prediabetes and hyperinsulinism; in these studies, Irs2 is required to maintain metabolic and pathological changes in adrenal gland medulla; deficiency of Irs2 leads to up-regulation of tyrosine hydroxylase and apoptosis in adrenomedullary chromaffin cells in this species.
DPP-4 inhibitor sitagliptin has effects on cardiac function, glycemia, and beta-cell function together with reducing S6K1 activation and IRS-1 and IRS-2 degradation in the obesity female mouse model
Downregulation of macrophage Irs2 by hyperinsulinemia impairs IL-4-indeuced M2a-subtype macrophage activation in obesity.
'selective insulin resistance' is caused by the differential expression of Irs1 and Irs2 in different zones of the liver
Lung-specific dual ablation of insulin receptor substrates 1/2 (succumb to tumor burdenIrs1/Irs2) strongly suppresses tumor initiation and dramatically extends the survival of a mouse model of lung cancer with Kras activation and p53 loss. Mice with Irs1/Irs2 loss eventually.
Insulin receptor substrate 2 (IRS2) is phosphorylated during induction of CAFLTP, a process that requires cytosolic free Ca2+.
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 sensing by NGNs and hyperphagic obese phenotype in IRS2 knockout mice
Mutation of five "inhibitory" Ser 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 and superoxide dismutase, and decreased nitric oxide synthase in 7- to 10-week-old IRS2(5A)-beta mice compared with IRS2(WT)-beta mice.
data identify SH2B1 as a major regulator of IRS2 stability, demonstrate a novel feedback mechanism linking mTORC1 signaling with IRS2, and identify 4E-BP2 as a major regulator of proliferation and survival of beta-cells.
Decreased miR-33 levels can up-regulate IRS-2 expression, which appears to compensate for the defects of the insulin signaling pathway in Irs-1 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 inhibitor and PPARgamma agonist exerts protective effects on pancreatic beta-cells in diabetic db/db 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 secretion.
Results indicate that although IRS isoforms (irs1 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.
The study identified the serine phosphorylation (p-Ser) sites induced by PKC-Beta activation or AGT, which inhibits insulin-induced p-Tyr 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