IRS1


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IRS1

A gene on chromosome 2q36 that encodes a protein phosphorylated by insulin receptor tyrosine kinase; it is thought to mediate the effects of insulin, insulin-like growth factor 1 and other cytokines by acting as a molecular adaptor between various receptor tyrosine kinases and downstream effectors.
 
Molecular pathology
IRS1 mutations are associated with type-2 diabetes and insulin resistance.
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Alterations in mRNA abundance for GLUT4, IRS1, ACACA, FASN, FATP2, CD36, and G6PC observed in adipose and liver tissues, coupled with elevated insulin and leptin in male offspring, provide further evidence for developmental programming of MS in this model, though as noted previously, exposure may have continued after birth due to placental or lactational transfer.
A replication study of the IRS1, CAPN10, TCF7L2, and PPARG gene polymorphisms associated with type 2 diabetes in two different populations of Mexico.
As a sex-specific interaction between the IRS1 variant rs2943641 and dietary factors on risk of type 2 diabetes was observed in a prior report (26), statistical analysis was performed in men and women separately in both BPRHS and MESA.
Additionally, exogenous factors like obesity may activate serine/threonine kinases that phosphorilate IRS1 and inhibit its function.
Known as IRS1, it is linked to an increased risk of Type 2 diabetes and heart disease.
Furthermore, in vitro studies revealed that treatment with chemerin induces insulin resistance in human skeletal muscle cells at the levels of IRS1 (Insulin receptor substrate 1), protein kinases B (PKB), and Glycogen synthase kinase 3 (GSK3) phosphorrylation and glucose uptake [11].
This appeared to influence a gene called insulin receptor substrate 1, or IRS1.
Importantly, when they added the gene for IRS1 back into the knockout cells, the precursors recovered most of their ability to differentiate into brown fat cells.
The insulin receptor substrates IRS1 and IRS2 bind to the activated insulin receptor and serve as adaptor molecules for the further propagation of signal transduction.
41] claimed that local OS increased IRS-1 and IRS-2 serine phosphorylations, decreased IRS1 protein content, and impaired insulin sensitivity in 3T3-L1 adipocytes.
Exogenous ER[alpha] reversed the I3C mediated loss of IGF1R and IRS1 gene expression demonstrating that down-regulation of ER[alpha] is functionally linked to I3C control of IGF1R and IRS1 expression.