抗体

Rabbit anti Phospho- IRS-1 (pSer 312) antibody

MBS462057

0.1毫克

350美元

多克隆

兔

未共轭

人类, 小鼠, 大鼠

免疫印迹, 酶联免疫吸附测定, 免疫组化

抗体

Rabbit anti Phospho- IRS-1 (pSer 312) antibody

IRS-1(pS312)

Rabbit anti-IRS-1 (p Ser312); Anti-phospho-IRS-1 (pSer312); Insulin-receptor substrate 1 (IRS-1).

Insulin receptor substrate 1; Insulin receptor substrate 1; insulin receptor substrate 1; IRS-1; OTTHUMP00000164234; insulin receptor substrate 1

IRS-1(pS312)

胰岛素受体底物1;胰岛素受体底物1;HIRS-1

IRS1_HUMAN

兔

人类, 大鼠, 小鼠

This antibody recognizes ~165 kDa of human IRS-1 (pSer312). It also reacts with mouse and rat. The other species are not tested.

The Rabbit IgG is purified by Site-specific Epitope Affinity Purification.

This affinity purified antibody is supplied in sterile Tris-buffered saline (pH7.2) containing antibody stabilizer

Size: 100 ug/200 ul

The antibodies are stable for 12 months from date of receipt when stored at -20 degree C to -70 degree C. The antibodies can be stored at 2 degree C-8 degree C for three month without detectable loss of activity. Avoid repeated freezing-thawing cycles.

酶联免疫吸附测定, 免疫印迹, 免疫组化

Western Blot: 0.1-1 ug/ml. ELISA: 0.01-0.1 ug/ml. Immunoprecipitation: 2-5 ug/ml. Immunohistochemistry: 0.5-2 ug/ml

Antigen Preparation: A synthetic peptide corresponding to the epitope ATSPA with a single phosphorylation site Ser 312 of human IRS-1.

Positive Control: CHO cell lysate

Insulin Receptor Substrate-1 (IRS-1), 165 kDa cytoplasmic docking protein, is one of the major endogenous substrates of the insulin receptor kinase. IRS-1 contains multiple tyrosine phosphorylation motifs that serve as docking sites for SH2 domain containing proteins, which mediate the metabolic and growth promoting functions of insulin. IRS-1 also contains over 30 potential serine/threonine phosphorylation sites. Ser312 of IRS-1 is phosphorylated by JNK and IKK and Ser789 is phosphorylated by SIK-2, a member of AMPK family. The phosphorylation of Tyr612 and Ser636/639 is mediated by the PKC and mTOR pathways, respectively and phosphorylation at Ser1101 is mediated by PKC, resulting in an inhibition of insulin signaling in the cell, suggesting a potential mechanism for insulin resistance in some models of obesity.

Li, Y. et al. (2004) J. Biol. Chem. 279, 45304-45307.

547738

P35568.1

P35568

P35568

165 kDa

Adipocytokine Signaling Pathway (83093); Adipocytokine Signaling Pathway (505); Adipogenesis Pathway (198832); Aldosterone-regulated Sodium Reabsorption Pathway (130626); Aldosterone-regulated Sodium Reabsorption Pathway (130590); Alpha6-Beta4 Integrin Signaling Pathway (198807); Downstream Signaling Of Activated FGFR Pathway (160957); EPO Receptor Signaling Pathway (198882); IGF1 Pathway (137992); IL-2 Signaling Pathway (198885)

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]

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. By similarity. Ref.28. Subunit structure: Interacts with UBTF and PIK3CA. By similarity. Interacts (via phosphorylated YXXM motifs) with PIK3R1. By similarity. Interacts with ROCK1. By similarity. Interacts (via PH domain) with PHIP. By similarity. Interacts with GRB2. By similarity. Interacts with SOCS7. Interacts (via IRS-type PTB domain) with IGF1R and INSR (via the tyrosine-phosphorylated NPXY motif). Ref.5 Ref.6 Ref.7 Ref.9. Post-translational modification: 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. By similarity.Phosphorylation of Tyr-896 is required for GRB2-binding. 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. Involvement in disease: Polymorphisms in IRS1 may be involved in the etiology of non-insulin-dependent diabetes mellitus (NIDDM) [. MIM:125853]. Ref.22 Ref.23 Ref.25 Ref.28 Ref.29. Sequence similarities: Contains 1 IRS-type PTB domain.Contains 1 PH domain.

0.1毫克

350美元