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IRS4 encodes the insulin receptor substrate 4, a cytoplasmic protein that contains many potential tyrosine and serine/threonine phosphorylation sites. Additionally we are shipping IRS4 Proteins (5) and IRS4 Kits (2) and many more products for this protein.
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these results demonstrated that miR (show MLXIP Antibodies)-493 acts as a tumor suppressor and inhibits cell proliferation and cell cycle in human melanoma by directly targeting IRS4.
The association of IRS4 with SSH1 (show SSH1 Antibodies) contributes to localized activation of cofilin (show CFL1 Antibodies) in membrane protrusions.
Overexpression of IRS4 in U2OS cells activates PI3K (show PIK3CA Antibodies) signalling.
We genotyped single-nucleotide polymorphisms of IGF1 (show IGF1 Antibodies), IGF2, IGF1R (show IGF1R Antibodies), IGF2R (show IGF2R Antibodies), IGFBP1 (show IGFBPI Antibodies), IGFBP3 (show IGFBP3 Antibodies), IGFBP5 (show IGFBP5 Antibodies), IRS1 (show IRS1 Antibodies), IRS2 (show IRS2 Antibodies), and IRS (show IARS Antibodies) in pancreatic cancer patients
This study clearly demonstrates associations between body mass index and IRS-4 variants in schizophrenia patients, but not in healthy controls, pointing to a possible involvement of IRS-4 in the control of body weight in schizophrenia.
Study for the first time identified IRS4 mutations in T-ALL.
IRS-4 gene is not of importance for aetiology of the vast majority of schizophrenia cases, but a single patient with schizophrenia and a mutation in IRS-4 points to that the insulin (show INS Antibodies) signalling system is of interest in the search for schizophrenia genes
The t(X;6) in subungual exostosis results in transcriptional deregulation of the gene for insulin receptor substrate 4.
Insulin receptor substrate 4 associates with the protein IRAS (show NISCH Antibodies)
IRS-4 does not function as a substrate of the insulin (show INS Antibodies) and the IGF-I receptor (show IGF1R Antibodies) in primary muscle cells but may be involved in nonreceptor tyrosine kinase (show TXK Antibodies) signaling.
conclude that Y103 is required for the internalization of hCTR1 (show SLC31A1 Antibodies) in response to Cu, that this occurs by a mechanism other than phosphorylation and that mutation of Y103 modulates the interaction with IRS-4
Down-regulation of the insulin receptor substrate 4 (Irs4) gene, may be an important event in the transition from age-related changes to Alzheimer's disease specific-changes.
These data suggest that IRS (show IARS Antibodies)-dependent signaling pathways work by recruiting different signaling molecules to determine specificity of IL-2R gamma (show IL2RG Antibodies) superfamily cytokines.
These data indicate that both insulin receptor (show INSR Antibodies) substrate (IRS)-1 (show IRS1 Antibodies) and -3, but not IRS-2 (show IRS2 Antibodies) or IRS-4, play key roles in the differentiation of brown adipocytes.
Data demonstrate that IRS4 interacts with the LR. This recruitment is leptin (show LEP Antibodies) dependent and requires phosphorylation of the Y1077 motif of the LR.
Protein kinase C-zeta (show PRKCZ Antibodies) phosphorylates insulin receptor substrate-1 (show IRS1 Antibodies), -3, and -4 but not -2 (show CNOT2 Antibodies).
IRS4 encodes the insulin receptor substrate 4, a cytoplasmic protein that contains many potential tyrosine and serine/threonine phosphorylation sites. Tyrosine-phosphorylated IRS4 protein has been shown to associate with cytoplasmic signalling molecules that contain SH2 domains. The IRS4 protein is phosphorylated by the insulin receptor tyrosine kinase upon receptor stimulation..
insulin receptor substrate 4
, 160 kDa phosphotyrosine protein
, phosphoprotein of 160 kDa
, insulin receptor substrate 2-A
, insulin receptor substrate protein
, insulin receptor substrate-undetermined designation
, insulin receptor substrate-unique