Stat5 is a physiological substrate of the insulin receptor.
about
Molecular basis of signaling specificity of insulin and IGF receptors: neglected corners and recent advancesThe SPOT technique as a tool for studying protein tyrosine phosphatase substrate specificitiesInsulin-like growth factor-I augments erythropoietin-induced proliferation through enhanced tyrosine phosphorylation of STAT5Interaction of human suppressor of cytokine signaling (SOCS)-2 with the insulin-like growth factor-I receptorAutoinhibition of the insulin-like growth factor I receptor by the juxtamembrane regionProtein kinase PKR is required for platelet-derived growth factor signaling of c-fos gene expression via Erks and Stat3.PI3K signaling and Stat92E converge to modulate glial responsiveness to axonal injuryStructural and biochemical evidence for an autoinhibitory role for tyrosine 984 in the juxtamembrane region of the insulin receptorSignal transducer and activator of transcription 5A/B in prostate and breast cancersIdentification of the rat adapter Grb14 as an inhibitor of insulin actionsInsulin inhibits growth hormone signaling via the growth hormone receptor/JAK2/STAT5B pathwayInsulin enhances growth hormone induction of the MEK/ERK signaling pathwayInsulin and GH signaling in human skeletal muscle in vivo following exogenous GH exposure: impact of an oral glucose loadGenomic structure, expression and characterization of a STAT5 homologue from pufferfish (Tetraodon fluviatilis).Identification of Stat 5B as a substrate of the insulin receptor.STAT signaling in the pathogenesis and treatment of cancerTranscriptional regulation of the cyclin D1 promoter by STAT5: its involvement in cytokine-dependent growth of hematopoietic cells.Intrasteric inhibition of ATP binding is not required to prevent unregulated autophosphorylation or signaling by the insulin receptor.RACK1, an insulin-like growth factor I (IGF-I) receptor-interacting protein, modulates IGF-I-dependent integrin signaling and promotes cell spreading and contact with extracellular matrix.RACK1 recruits STAT3 specifically to insulin and insulin-like growth factor 1 receptors for activation, which is important for regulating anchorage-independent growth.Signaling by vitamin A and retinol-binding protein regulates gene expression to inhibit insulin responses.Hepatic oxidative stress promotes insulin-STAT-5 signaling and obesity by inactivating protein tyrosine phosphatase N2Signaling by vitamin A and retinol-binding protein in regulation of insulin responses and lipid homeostasis.Novel roles for insulin receptor (IR) in adipocytes and skeletal muscle cells via new and unexpected substrates.JAK-STAT signaling and myocardial glucose metabolism.Inputs and outputs of insulin receptor.Insulin and IGFs in obesity-related breast cancer.Modulation of the action of insulin by angiotensin-(1-7).Constitutive activation of STAT-3 and downregulation of SOCS-3 expression induced by adrenalectomy.A STAT inhibitor patent review: progress since 2011.TNF down-regulation of receptor tyrosine kinase-dependent mitogenic signal pathways as an important step in cytostasis induction and commitment to apoptosis of Kym-1 rhabdomyosarcoma cells.Impairment of hepatic growth hormone and glucocorticoid receptor signaling causes steatosis and hepatocellular carcinoma in mice.STAT5a activation mediates the epithelial to mesenchymal transition induced by oncogenic RhoAMatrix-independent activation of phosphatidylinositol 3-kinase, Stat3, and cyclin A-associated Cdk2 Is essential for anchorage-independent growth of v-Ros-transformed chicken embryo fibroblasts.Insulin Induction of SOCS-2 and SOCS-3 mRNA expression in C2C12 Skeletal Muscle Cells Is Mediated by Stat5*.Differential requirements of the MAP kinase and PI3 kinase signaling pathways in Src- versus insulin and IGF-1 receptors-induced growth and transformation of rat intestinal epithelial cells.Ethanol potentiates the stimulatory effects of insulin and phosphocholine on mitogenesis by a zinc-dependent and rapamycin-sensitive mechanism in fibroblasts and JB6 cells.Platelet-derived growth factor (PDGF)-induced activation of signal transducer and activator of transcription (Stat) 5 is mediated by PDGF beta-receptor and is not dependent on c-src, fyn, jak1 or jak2 kinases.STAT activation by the PDGF receptor requires juxtamembrane phosphorylation sites but not Src tyrosine kinase activation.Stat3 plays an important role in oncogenic Ros- and insulin-like growth factor I receptor-induced anchorage-independent growth.
P2860
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P2860
Stat5 is a physiological substrate of the insulin receptor.
description
1997 nî lūn-bûn
@nan
1997年の論文
@ja
1997年論文
@yue
1997年論文
@zh-hant
1997年論文
@zh-hk
1997年論文
@zh-mo
1997年論文
@zh-tw
1997年论文
@wuu
1997年论文
@zh
1997年论文
@zh-cn
name
Stat5 is a physiological substrate of the insulin receptor.
@ast
Stat5 is a physiological substrate of the insulin receptor.
@en
type
label
Stat5 is a physiological substrate of the insulin receptor.
@ast
Stat5 is a physiological substrate of the insulin receptor.
@en
prefLabel
Stat5 is a physiological substrate of the insulin receptor.
@ast
Stat5 is a physiological substrate of the insulin receptor.
@en
P2093
P2860
P356
P1476
Stat5 is a physiological substrate of the insulin receptor.
@en
P2093
P2860
P304
P356
10.1073/PNAS.94.6.2295
P407
P577
1997-03-01T00:00:00Z