IRS-1 (phospho-S323) polyclonal Antibody | BS4271

IRS-1 (phospho-S323) polyclonal Antibody | BS4271 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human,Mouse,Rat

Application: WB IHC IF

Application Range: WB: 1:500~1:1000 IHC: 1:50~1:200 IF: 1:50~1:200

Background: IRS-1, a major substrate of the insulin receptor, is phosphorylated in response to stimulation of cells by insulin, insulin-like growth factor 1 (IGF-1) and interleukin 4 (IL-4) . IRS-1 is phosphorylated on serine, threonine and tyrosine residues in a variety of tissues. An insulin-sensitive serine/threonine kinase casein kinase II mediates a portion of the insulin-stimulated serine/threonine phosphorylation of overexpressed IRS-1 in vivo. Thr 502 is identified as the major casein kinase II-catalyzed phosphorylation site in rat IRS-1, and Ser 99 is an additional phosphorylation site catalyzed by casein kinase II. Thus, casein kinase II-catalyzed phosphorylation of IRS-1 may be a component of the intracellular insulin signaling cascade. IRS-1 contains three putative binding sites for 14-3-3 (Ser 270, Ser 374 and Ser 641) and the motif around Ser 270 is located in the phosphortyrosine binding domain of IRS-1, which is responsible for the interaction with the insulin receptor.

Storage & Stability: Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze-thaw cycles.

Specificity: p-IRS-1 (S323) polyclonal Antibody detects endogenous levels of IRS-1 only when phosphorylated at Ser323.

Molecular Weight: ~ 132, 180 kDa

Note: For research use only, not for use in diagnostic procedure.

Alternative Names: Insulin receptor substrate 1; IRS-1; IRS1

Immunogen: Synthetic phosphopeptide derived from human IRS-1 around the phosphorylation site of Serine 323.

Conjugate: Unconjugated

Modification: Phosphorylation

Purification & Purity: The Antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen and the purity is > 95% (by SDS-PAGE) .

Pathway: Examples of Crosstalk Between Post-translational Modifications,Cell Cycle G2 M DNA Damage Signaling Pathway,