Western Blotting (WB), ELISA, Immunofluorescence (IF), Immunocytochemistry (ICC)
Purification
IRS-1 Antibody is affinity chromatography purified via peptide column.
Immunogen
IRS-1 antibody was raised against a 16 amino acid synthetic peptide from near the center of human IRS-1. The immunogen is located within amino acids 910 - 960 of IRS-1.
IRS1
Reactivity: Human
WB, IHC, ELISA, IF
Host: Rabbit
Polyclonal
unconjugated
Application Notes
IRS-1antibody can be used for the detection of IRS-1 by Western blot at 1 - 4 μ,g/mL. Antibody can also be used for immunocytochemistry starting at 2 μ,g/mL. For immunofluorescence start at 2 μ,g/mL.
Antibody validated: Western Blot in human samples, Immunocytochemistry in mouse samples and Immunofluorescence in mouse samples. All other applications and species not yet tested.
Restrictions
For Research Use only
Format
Liquid
Concentration
1 mg/mL
Buffer
IRS-1 Antibody is supplied in PBS containing 0.02 % sodium azide.
Preservative
Sodium azide
Precaution of Use
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Storage
-20 °C,4 °C
Storage Comment
IRS-1 antibody can be stored at 4°C for three months and -20°C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
IRS-1 Antibody: Following tyrosine phosphorylation, the insulin receptor substrate 1 and 2 (IRS-1 and IRS-2) can form a protein scaffolding for the assembly of a host of Src homology 2 (SH2) domain-containing proteins. IRS-1 tyrosine phosphorylation can occur through the activity of several cytokine and growth factor receptors such as interleukin (IL)-4, IL-9, interferon-gamma, in addition to the insulin and insulin-like growth factor 1 receptors. The scaffolding provided by IRS-1 and IRS-2 is necessary for insulin signal transduction across the cell membrane. IRS-1 tyrosine phosphorylation, and thus formation of the IRS scaffolding is inhibited by tumor necrosis factor (TNF), and this inhibition can itself be blocked by rapamycin, an inhibitor of the mammalian target of rapamycin (TOR). TNF activity could also be blocked by inhibition of the Akt kinase and the PTEN tumor suppressor, suggesting that TNF impairs insulin signaling through IRS-1 by activation of the TOR signaling pathway.