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Details for Product No. ABIN196981

Insulin Receptor Substrate 1 (IRS1) (pSer639) antibody

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Antigen
Synonyms HIRS-1, G972R, IRS-1, IRS1IRM, irs1, irsu, IRS1
Epitope
»Alternatives pSer639
Reactivity
»Alternatives Human, Mouse (Murine), Rat (Rattus)
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. ABIN196981
Quantity 50 µg
Price
275.00 $   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 639 (P-K-Sp-V-S).
Specificity This antibody detects endogenous levels of IRS-1 only when phosphorylated at Serine 639.
Purification 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: 1/500~1/10000. Immunohistochemistry on Paraffin Sections: 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 1.0 mg/mL
Buffer BPS (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
Storage Comment Store the antibody (in aliquots) at -20°C.
Expiry Date 12 months
Background publications 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).

Batty, Fleming, Downes: "Muscarinic-receptor-mediated inhibition of insulin-like growth factor-1 receptor-stimulated phosphoinositide 3-kinase signalling in 1321N1 astrocytoma cells." in: The Biochemical journal, Vol. 379, Issue Pt 3, pp. 641-51, 2004 (PubMed).

Steppan, Wang, Whiteman et al.: "Activation of SOCS-3 by resistin." in: Molecular and cellular biology, Vol. 25, Issue 4, pp. 1569-75, 2005 (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), (335), (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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