Anti-Human Insulin Receptor Substrate-1 (IRS-1)

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Pricing & Details

Product No.I-465
Protein
Insulin Receptor Substrate-1
Formats AvailableView All
Product Type
Polyclonal Antibody
Applications
IHC FFPE
,
WB
Prod No.
Size
Price
Avail.
Qty
Add to cart
I-465-20ug
20 µg
$195.00
In stock
Max:
Min: 1
Step: 1
I-465-0.1 mg
0.1 mg
$397.00
In stock
Max:
Min: 1
Step: 1
Bulk quantities available. Contact us for pricing.

Data

Antibody Details

Product Details

Reactivity Species
Human
Host Species
Rabbit
Immunogen
PN:I-482
Product Concentration
0.5 mg/ml
Formulation
This polyclonal antibody is formulated in phosphate buffered saline (PBS) pH 7.4 containing 0.02% sodium azide as a preservative.
Storage and Handling
This polyclonal antibody is stable for at least one week when stored at 2-8°C. For long term storage, aliquot in working volumes without diluting and store at –20°C in a manual defrost freezer. Avoid Repeated Freeze Thaw Cycles.
Country of Origin
USA
Shipping
Next Day Ambient
Each investigator should determine their own optimal working dilution for specific applications. See directions on lot specific datasheets, as information may periodically change.

Description

Specificity
Rabbit Anti-Human Insulin Receptor Substrate-1 (IRS-1) recognizes Human and Mouse IRS-1. This polyclonal antibody was purified using affinity chromatography.
Background
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.1 IRS-1 tyrosine phosphorylation can occur through the activity of several cytokine and growth factor receptors such as interleukin (IL)-4, IL-9, interferon-α, in addition to the insulin and insulin-like growth factor 1 receptors.2 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)>3,4 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.3

Antigen Details

References & Citations

1. Giovannone, B. et al. (2000) Diabetes Metab. Res. Rev. 16:434
2. Waters, SB. et al. (1996) Trends in Cell Biol. 6:1
3. Ozes, ON. et al. (2001) Proc. Natl. Acad. Sci. USA 98:4640
4. Shamji, AF. et al. (2003) Mol. Cell 12:271
IHC
General Western Blot Protocol
Products are for research use only. Not for use in diagnostic or therapeutic procedures.
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