IRS1 (17G5) Rabbit Monoclonal Antibody

Product Information
Application Applications Legend: E=ELISA WB=Western Blotting IHC=Immunohistochemistry IHC-P=Immunohistochemistry (Paraffin) IP=Immunoprecipitation IF=Immunofluorescence IC=Immunochemistry ICC=Immunocytochemistry FC=Flow Cytometry DB=Dot Blot	WB, IHC-P, ICC, FC, IF
Primary Accession	P35568
Reactivity	Human
Clonality	Monoclonal
Calculated MW	131591 Da

Additional Information
Gene ID	3667
Other Names	Insulin receptor substrate 1, IRS-1, IRS1
Dilution	WB~~1:1000 IHC-P~~1:50~200 ICC~~N/A FC~~1:10~50 IF~~1:50~200
Storage Conditions	-20℃

For Research Use Only. Not For Use In Diagnostic Procedures.

Protein Information
Name	IRS1
Function	Signaling adapter protein that participates in the signal transduction from two prominent receptor tyrosine kinases, insulin receptor/INSR and insulin-like growth factor I receptor/IGF1R (PubMed:7541045, PubMed:33991522, PubMed:38625937). Plays therefore an important role in development, growth, glucose homeostasis as well as lipid metabolism (PubMed:19639489). Upon phosphorylation by the insulin receptor, functions as a signaling scaffold that propagates insulin action through binding to SH2 domain-containing proteins including the p85 regulatory subunit of PI3K, NCK1, NCK2, GRB2 or SHP2 (PubMed:11171109, PubMed:8265614). Recruitment of GRB2 leads to the activation of the guanine nucleotide exchange factor SOS1 which in turn triggers the Ras/Raf/MEK/MAPK signaling cascade (By similarity). Activation of the PI3K/AKT pathway is responsible for most of insulin metabolic effects in the cell, and the Ras/Raf/MEK/MAPK is involved in the regulation of gene expression and in cooperation with the PI3K pathway regulates cell growth and differentiation. Acts a positive regulator of the Wnt/beta-catenin signaling pathway through suppression of DVL2 autophagy-mediated degradation leading to cell proliferation (PubMed:24616100).
Cellular Location	Cytoplasm. Nucleus. Note=Nuclear or cytoplasmic localization of IRS1 correlates with the transition from proliferation to chondrogenic differentiation.