BD-PP0881

IRS-1 (phospho Ser323) Rabbit Polyclonal Antibody

IRS1; Insulin receptor substrate 1; IRS-1

常规抗体

IRS1

Insulin receptor substrate 1

WB

Human,Mouse,Rat,Monkey

1 mg/ml

Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% New type preservative N.

3667

http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&term=3667

P35568

http://www.uniprot.org/uniprotkb/P35568/entry

16367

http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&term=16367

P35569

http://www.uniprot.org/uniprot/P35569

25467

http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&term=25467

P35570

http://www.uniprot.org/uniprot/P35570

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.

WB 1:500 - 1:2000. IHC 1:100 - 1:300. IF 1:200 - 1:1000. ELISA: 1:10000. Not yet tested in other applications.

170kD

-20°C/1 year

Polyclonal, Rabbit,IgG

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],

Epithelium,Eye,Skeletal muscle,

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

Neurotrophin;Insulin_Receptor;Adipocytokine;Type II diabetes mellitus;Aldosterone-regulated sodium reabsorption;

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.,

现货

The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.