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IRS4 encodes the insulin receptor substrate 4, a cytoplasmic protein that contains many potential tyrosine and serine/threonine phosphorylation sites. De plus, nous expédions IRS4 Protéines (5) et IRS4 Kits (3) et beaucoup plus de produits pour cette protéine.
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IRS4 overexpression is associated with cancer.
these results demonstrated that miR (Montrer MLXIP Anticorps)-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 (Montrer SSH1 Anticorps) contributes to localized activation of cofilin (Montrer CFL1 Anticorps) in membrane protrusions.
Overexpression of IRS4 in U2OS cells activates PI3K (Montrer PIK3CA Anticorps) signalling.
We genotyped single-nucleotide polymorphisms of IGF1 (Montrer IGF1 Anticorps), IGF2, IGF1R (Montrer IGF1R Anticorps), IGF2R (Montrer IGF2R Anticorps), IGFBP1 (Montrer IGFBPI Anticorps), IGFBP3 (Montrer IGFBP3 Anticorps), IGFBP5 (Montrer IGFBP5 Anticorps), IRS1 (Montrer IRS1 Anticorps), IRS2 (Montrer IRS2 Anticorps), and IRS (Montrer IARS Anticorps) 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 (Montrer INS Anticorps) 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 (Montrer NISCH Anticorps)
conclude that Y103 is required for the internalization of hCTR1 (Montrer SLC31A1 Anticorps) 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 (Montrer IARS Anticorps)-dependent signaling pathways work by recruiting different signaling molecules to determine specificity of IL-2R gamma (Montrer IL2RG Anticorps) superfamily cytokines.
These data indicate that both insulin receptor (Montrer INSR Anticorps) substrate (IRS)-1 (Montrer IRS1 Anticorps) and -3, but not IRS-2 (Montrer IRS2 Anticorps) or IRS-4, play key roles in the differentiation of brown adipocytes.
Data demonstrate that IRS4 interacts with the LR. This recruitment is leptin (Montrer LEP Anticorps) dependent and requires phosphorylation of the Y1077 motif of the LR.
Protein kinase C-zeta (Montrer PRKCZ Anticorps) phosphorylates insulin receptor substrate-1 (Montrer IRS1 Anticorps), -3, and -4 but not -2 (Montrer CNOT2 Anticorps).
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