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Details for Product No. ABIN196978

Insulin Receptor Substrate 1 (IRS1) (pSer636) antibody

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Antigen
Synonyms HIRS-1, G972R, IRS-1, IRS1IRM, irs1, irsu, IRS1
Epitope
»Alternatives pSer636
Reactivity
»Alternatives Human, Mouse (Murine)
Host
»Alternatives Rabbit
Clonality Polyclonal
Conjugate
»Alternatives Un-conjugated
Application
»Alternatives Western Blotting (WB), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p))
Pubmed 4 references available
Catalog no. ABIN196978
Quantity 0.1 mg
Price
346.50 $   Plus shipping costs $45.00
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Availability Will be delivered in 6 to 8 Business Days
Immunogen The antiserum was produced against synthesized phosphopeptide derived from human IRS-1 around the phosphorylation site of serine 636 (P-M-SP-P-K).
Specificity IRS-1 antibody detects endogenous levels of IRS-1 only when phosphorylated at serine 636.
Purification The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific phosphopeptide. The antibody against non-phosphopeptide was removed by chromatography using non-phosphopeptide corresponding to the phosphorylation site.
Alternative Name IRS1
Background Insulin receptor substrates (IRS) are responsible for several insulin related activities, such as glucose homeostasis, cell growth, cell transformation, apoptosis and insulin signal transduction. Serine/threonine phosphorylation of IRS1 has been demonstrated to be a negative regulator of insulin signaling and is responsible for its degradation, although IRS1 degradation pathways are not well understood. IRS1 has also been shown to be constitutively activated in cancers such as breast cancer, Wilm's tumors, and adrenal cortical carcinomas, thus making IRS1 phosphorylation and subsequent degradation an attractive therapeutic target. To date there have been four subtypes identified: IRS1, 2, 3 and 4, with IRS1 being widely expressed.
Alternate names: IRS-1, Insulin receptor substrate 1
Gene ID 3667
NCBI Accession NP_005535.1
UniProt P35568
Research Area Cardiovascular, Atherosclerosis, Signaling, Growth Factors, Cancer
Application Notes Western Blot: 1: 500~1: 1000. Immunohistochemistry: 1: 50-1: 100. Other applications not tested. Optimal dilutions are dependent on conditions and should be determined by the user.
Restrictions For Research Use only
Format Liquid
Concentration 1.0mg/mL
Buffer PBS(without Mg2+ and Ca2+), pH 7.4 containing 150mM NaCl, 0.02% sodium azide and 50% glycerol
Preservative Sodium azide
Handling Advice Avoid repeated freezing and thawing.
Storage -20 °C
Expiry Date 12 months
Background publications Szanto, Kahn: "Selective interaction between leptin and insulin signaling pathways in a hepatic cell line." in: Proceedings of the National Academy of Sciences of the United States of America, Vol. 97, Issue 5, pp. 2355-60, 2000 (PubMed).

Kadowaki: "Insights into insulin resistance and type 2 diabetes from knockout mouse models." in: The Journal of clinical investigation, Vol. 106, Issue 4, pp. 459-65, 2000 (PubMed).

Ozes, Akca, Mayo et al.: "A phosphatidylinositol 3-kinase/Akt/mTOR pathway mediates and PTEN antagonizes tumor necrosis factor inhibition of insulin signaling through insulin receptor substrate-1." in: Proceedings of the National Academy of Sciences of the United States of America, Vol. 98, Issue 8, pp. 4640-5, 2001 (PubMed).

Tzatsos, Kandror: "Nutrients suppress phosphatidylinositol 3-kinase/Akt signaling via raptor-dependent mTOR-mediated insulin receptor substrate 1 phosphorylation." in: Molecular and cellular biology, Vol. 26, Issue 1, pp. 63-76, 2005 (PubMed).

Alternatives for antigen "Insulin Receptor Substrate 1 (IRS1)", type "Antibodies"
Hosts (454), (15)
Reactivities (439), (351), (336), (132), (121), (97), (77), (36), (1)
Applications (259), (162), (128), (120), (100), (67), (33), (24), (6), (4), (1)
Conjugates (13), (12), (12), (12), (12), (12), (12), (12), (12), (12), (12)
Epitopes (37), (36), (35), (34), (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)
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