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IRS4 encodes the insulin receptor substrate 4, a cytoplasmic protein that contains many potential tyrosine and serine/threonine phosphorylation sites. 再加上，我们可以发IRS4 蛋白 (7) 和 IRS4 试剂盒 (5)和数多这个蛋白质的别的产品。
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increase of IRS-4 expression may be involved to some extent in colorectal cancer.
IRS4 overexpression is associated with cancer.
these results demonstrated that miR (显示 MLXIP 抗体)-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 (显示 SSH1 抗体) contributes to localized activation of cofilin (显示 CFL1 抗体) in membrane protrusions.
Overexpression of IRS4 in U2OS cells activates PI3K (显示 PIK3CA 抗体) signalling.
We genotyped single-nucleotide polymorphisms of IGF1 (显示 IGF1 抗体), IGF2, IGF1R (显示 IGF1R 抗体), IGF2R (显示 IGF2R 抗体), IGFBP1 (显示 IGFBPI 抗体), IGFBP3 (显示 IGFBP3 抗体), IGFBP5 (显示 IGFBP5 抗体), IRS1 (显示 IRS1 抗体), IRS2 (显示 IRS2 抗体), and IRS (显示 IARS 抗体) 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 (显示 INS 抗体) 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.
conclude that Y103 is required for the internalization of hCTR1 (显示 SLC31A1 抗体) 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 (显示 IARS 抗体)-dependent signaling pathways work by recruiting different signaling molecules to determine specificity of IL-2R gamma (显示 IL2RG 抗体) superfamily cytokines.
These data indicate that both insulin receptor (显示 INSR 抗体) substrate (IRS)-1 (显示 IRS1 抗体) and -3, but not IRS-2 (显示 IRS2 抗体) or IRS-4, play key roles in the differentiation of brown adipocytes.
Data demonstrate that IRS4 interacts with the LR. This recruitment is leptin (显示 LEP 抗体) dependent and requires phosphorylation of the Y1077 motif of the LR.
Protein kinase C-zeta (显示 PRKCZ 抗体) phosphorylates insulin receptor substrate-1 (显示 IRS1 抗体), -3, and -4 but not -2 (显示 CNOT2 抗体).
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