The antiserum was produced against synthesized peptide derived from human IRS-1 around the phosphorylation site of Ser323. AA range:289-338

Phospho-IRS-1 (S323) Polyclonal Antibody detects endogenous levels of IRS-1 protein only when phosphorylated at S323.The name of modified sites may be influenced by many factors, such as species (the modified site was not originally found in human samples) and the change of protein sequence (the previous protein sequence is incomplete, and the protein sequence may be prolonged with the development of protein sequencing technology). When naming, we will use the "numbers" in historical reference to keep the sites consistent with the reports. The antibody binds to the following modification sequence (lowercase letters are modification sites):PGsFR

IRS1

Insulin receptor substrate 1

IRS1 ;
Insulin receptor substrate 1 ;
IRS-1

This gene encodes a protein which is phosphorylated by insulin receptor tyrosine kinase. Mutations in this gene are associated with type II diabetes and susceptibility to insulin resistance. [provided by RefSeq, Nov 2009],

Disease:Polymorphisms in IRS1 may be involved in the etiology of non-insulin-dependent diabetes mellitus (NIDDM) [MIM:125853].,Function:May mediate the control of various cellular processes by insulin. When phosphorylated by the insulin receptor binds specifically to various cellular proteins containing SH2 domains such as phosphatidylinositol 3-kinase p85 subunit or GRB2. Activates phosphatidylinositol 3-kinase when bound to the regulatory p85 subunit.,polymorphism:The Arg-971 polymorphism impairs the ability of insulin to stimulate glucose transport, glucose transporter translocation, and glycogen synthesis by affecting the PI3K/AKT1/GSK3 signaling pathway. The polymorphism at Arg-971 may contribute to the in vivo insulin resistance observed in carriers of this variant. Arg-971 could contribute to the risk for atherosclerotic cardiovascular diseases associated with non-insulin-dependent diabetes mellitus (NIDDM) by producing a cluster of insulin resistance-related metabolic abnormalities. In insulin-stimulated human endothelial cells from carriers of the Arg-971 polymorphism, genetic impairment of the IRS1/PI3K/PDPK1/AKT1 insulin signaling cascade results in impaired insulin-stimulated nitric oxide (NO) release and suggested that this may be a mechanism through which the Arg-971 polymorphism contributes to the genetic predisposition to develop endothelial dysfunction and cardiovascular disease. The Arg-971 polymorphism not only reduces phosphorylation of the substrate but allows IRS1 to act as an inhibitor of PI3K, producing global insulin resistance.,PTM:Phosphorylation of Tyr-896 is required for GRB2-binding.,PTM:Serine phosphorylation of IRS1 is a mechanism for insulin resistance. Ser-312 phosphorylation inhibits insulin action through disruption of IRS1 interaction with the insulin receptor.,similarity:Contains 1 IRS-type PTB domain.,similarity:Contains 1 PH domain.,subunit:Interacts with the NPXY motif of tyrosine-phosphorylated IGF1R and INSR via the PTB domain. Binds to phosphatidylinositol 3-kinase p85 subunit via the phosphorylated YXXM motifs. Binds ROCK1. Binds to UBTF and PIK3CA in nuclear extracts (By similarity). Interacts with SOCS7.,

nucleus,cytoplasm,cytosol,plasma membrane,insulin receptor complex,caveola,intracellular membrane-bounded organelle,

Epithelium,Eye,Skeletal muscle,

>>cGMP-PKG signaling pathway ;
>>FoxO signaling pathway ;
>>Autophagy - animal ;
>>mTOR signaling pathway ;
>>PI3K-Akt signaling pathway ;
>>AMPK signaling pathway ;
>>Longevity regulating pathway ;
>>Longevity regulating pathway - multiple species ;
>>Neurotrophin signaling pathway ;
>>Insulin signaling pathway ;
>>Adipocytokine signaling pathway ;
>>Regulation of lipolysis in adipocytes ;
>>Type II diabetes mellitus ;
>>Insulin resistance ;
>>Non-alcoholic fatty liver disease ;
>>Growth hormone synthesis, secretion and action ;
>>Aldosterone-regulated sodium reabsorption ;
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