|Application ||WB, IHC|
|Calculated MW||131591 Da|
|Other Names||Insulin receptor substrate 1, IRS-1, IRS1|
|Target/Specificity||A synthetic peptide corresponding to residues near the C-terminus of human IRS-1was used as immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||IRS-1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|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).|
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Provided below are standard protocols that you may find useful for product applications.
Insulin receptor substrates (IRS), the major intracellular substrates of the insulin receptor (IR), are adaptor proteins that transduce signals from the IR to downstream effectors that are important for the biological effect of insulin (1-2). After insulin stimulation, IRS proteins are rapidly phosphorylated on multiple tyrosine residues. Once phosphorylated, IRS proteins bind and activate Grb-2, SHP2 and the PI3-K p85 subunit (2-3). IRS-1 functions as one of the key regulators of IR and the insulin-like growth factor-1 receptor. Disruption of IRS-1 causes growth retardation and insulin resistance associated with hypertension, hypertriglyceridemia, and impaired endothelium-dependent vascular relaxation (4-5)
1. Sun XJ, Rothenberg P, Kahn CR, et al. 1991 Nature. 352:73
2. White MF. 1997 Diabetologia. 40:S2
3. Virkamaki, A., Ueki, K., and Kahn, C. R. (1999) J. Clin. Investig. 103, 931
4. Araki E, Lipes MA, Patti ME, et al. 1994 Nature. 372:186
5. Abe H, Yamada N, Kamata K, et al. 1998 J Clin Invest. 101:1784
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