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Details for Product No. ABIN968515

Insulin Receptor Substrate 1 (IRS1) (AA 1131-1234) antibody

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Synonyms HIRS-1, G972R, IRS-1, IRS1IRM, irs1, irsu, IRS1
»Alternatives AA 1131-1234
»Alternatives Rat (Rattus)
»Alternatives Mouse
Clonality (Clone) Monoclonal ()
»Alternatives Un-conjugated
»Alternatives Western Blotting (WB), Immunofluorescence (IF)
Pubmed 5 references available
Catalog no. ABIN968515
Quantity 150 µg
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Immunogen Rat IRS-1
Clone 6
Isotype IgG1
Cross-Reactivity Mouse (Murine)
Characteristics 1. Since applications vary, each investigator should titrate the reagent to obtain optimal results.
2. Please refer to us for technical protocols.
3. Source of all serum proteins is from USDA inspected abattoirs located in the United States.
4. Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
Purification Purified from tissue culture supernatant or ascites by affinity chromatography.
Purity Purified
Alternative Name IRS-1
Background The IRS (Insulin receptor substrate) proteins IRS-1, IRS-2, IRS-3, and IRS-4 are major substrates of the insulin receptor tyrosine kinase and the insulin-like growth factor-1 receptor. IRS proteins contain an N-terminal pleckstrin homology (PH) domain, an ATP-binding domain, and multiple tyrosine phosphorylation sites in the C-terminus. Following insulin receptor ligation, IRS-1 binds to the juxtamembrane region of the receptor and is tyrosine phosphorylated. This facilitates its interaction with SH2 domain-containing signaling proteins, such as PI3 kinase, fyn, Grb2, and PTP1D. Phosphorylation dramatically reduces the affinity of IRS-1 for the insulin receptor, indicating that dissociation from the receptor and subsequent subcellular translocation are important to IRS-1 function in the pleiotropic effects induced by insulin. In support of this, IRS-1-null mice are viable, but exhibit growth retardation and abnormal glucose metabolism. In cases of reduced IRS-1 expression, certain IRS-1 functions can be assumed by the related IRS-2 protein, while other activities linked to IRS-1 are inhibited. Thus, IRS-1 is an essential component of insulin induced signal transduction. This antibody is routinely tested by western blot analysis.
Molecular Weight 180 kDa

Related Products: ABIN967389

Restrictions For Research Use only
Format Liquid
Concentration 250 µg/ml
Buffer Aqueous buffered solution containing BSA, glycerol.
Preservative Sodium azide
Storage -20 °C
Product cited in: Backer, Myers, Shoelson et al.: "Phosphatidylinositol 3'-kinase is activated by association with IRS-1 during insulin stimulation." in: The EMBO journal, Vol. 11, Issue 9, pp. 3469-79, 1992 (PubMed).

Sun, Rothenberg, Kahn et al.: "Structure of the insulin receptor substrate IRS-1 defines a unique signal transduction protein." in: Nature, Vol. 352, Issue 6330, pp. 73-7, 1991 (PubMed).

Kuhné, Zhao, Rowles et al.: "Dephosphorylation of insulin receptor substrate 1 by the tyrosine phosphatase PTP2C." in: The Journal of biological chemistry, Vol. 269, Issue 22, pp. 15833-7, 1994 (PubMed).

Paz, Liu, Shorer et al.: "Phosphorylation of insulin receptor substrate-1 (IRS-1) by protein kinase B positively regulates IRS-1 function." in: The Journal of biological chemistry, Vol. 274, Issue 40, pp. 28816-22, 1999 (PubMed).

Obici, Feng, Karkanias et al.: "Decreasing hypothalamic insulin receptors causes hyperphagia and insulin resistance in rats." in: Nature neuroscience, Vol. 5, Issue 6, pp. 566-72, 2002 (PubMed).

Alternatives for antigen "Insulin Receptor Substrate 1 (IRS1)", type "Antibodies"
Hosts (455), (15)
Reactivities (440), (352), (336), (132), (121), (97), (77), (36), (1)
Applications (260), (162), (128), (120), (101), (67), (33), (24), (6), (4), (1)
Conjugates (13), (12), (12), (12), (12), (12), (12), (12), (12), (12), (12)
Epitopes (37), (36), (35), (35), (23), (17), (17), (16), (16), (13), (13), (12), (12), (12), (12), (12), (6), (6), (6), (4), (4), (4), (4), (4), (4), (3), (3), (3), (2), (2), (2), (2), (2), (2), (2), (2), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1)