CST, 2384S, Phospho-IRS-1 (Ser302) Antibody

Polyclonal Antibody for studying IRS-1 (Ser307) phosphate. Validated for Western Blotting. Highly specific and rigorously validated in-house, Phospho-IRS-1 (Ser302) Antibody (CST #2384) is ready to ship. Product Usage Information Western Blotting: 1:1000 Storage Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at -20°C. Do not aliquot the antibody. Protocol Available protocols: Western Blotting Specificity / Sensitivity Phospho-IRS-1 (Ser302) Antibody detects endogenous levels of IRS-1 only when phosphorylated at Ser302 of mouse IRS-1 or Ser307 of human IRS-1. This antibody does not detect IRS-1 phosphorylated at other sites. Species Reactivity: Human, Mouse, Rat Source / Purification Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser 302 of mouse IRS-1. Antibodies are purified by protein A and peptide affinity chromatography. Background Insulin receptor substrate 1 (IRS-1) is one of the major substrates of the insulin receptor kinase (1). IRS-1 contains multiple tyrosine phosphorylation motifs that serve as docking sites for SH2-domain containing proteins that mediate the metabolic and growth-promoting functions of insulin (2-4). IRS-1 also contains over 30 potential serine/threonine phosphorylation sites. Ser307 of IRS-1 is phosphorylated by JNK (5) and IKK (6) while Ser789 is phosphorylated by SIK-2, a member of the AMPK family (7). The PKC and mTOR pathways mediate phosphorylation of IRS-1 at Ser612 and Ser636/639, respectively (8,9). Phosphorylation of IRS-1 at Ser1101 is mediated by PKCθ and results in an inhibition of insulin signaling in the cell, suggesting a potential mechanism for insulin resistance in some models of obesity (10). Ser302 in rat/mouse IRS-1 (corresponding to Ser307 of human IRS-1) is phosphorylated rapidly during insulin stimulation and has a postive role in IRS-1 tyrosine phosphorylation. Inhibition of Ser302 phosphorylation by short-term amino acid/glucose starvation correlates with a decrease in IRS-1 tyrosine phosphorylation without inhibition of insulin receptor autophosphorylation or Akt phosphorylation. A defect in this positive regulatory pathway may be a mechanism contributing to insulin resistence (11). Alternate Names HIRS-1; Insulin receptor substrate 1; IRS-1; IRS1 Specification REACTIVITY: H M R SENSITIVITY: Endogenous MW (kDa): 180 SOURCE: Rabbit