Osmotic shock inhibits insulin signaling by maintaining Akt/protein kinase B in an inactive dephosphorylated state
about
Hyperosmotic stress inhibits insulin receptor substrate-1 function by distinct mechanisms in 3T3-L1 adipocytesModulation of gene expression profiles by hyperosmolarity and insulinDomain swapping used to investigate the mechanism of protein kinase B regulation by 3-phosphoinositide-dependent protein kinase 1 and Ser473 kinaseHyperosmotic stress stimulates promoter activity and regulates cellular utilization of the serum- and glucocorticoid-inducible protein kinase (Sgk) by a p38 MAPK-dependent pathway.3-phosphoinositide-dependent protein kinase 1, an Akt1 kinase, is involved in dephosphorylation of Thr-308 of Akt1 in Chinese hamster ovary cells.Intramolecular and intermolecular interactions of protein kinase B define its activation in vivoProtein phosphatase 2A acts as a mitogen-activated protein kinase kinase kinase 3 (MEKK3) phosphatase to inhibit lysophosphatidic acid-induced IkappaB kinase beta/nuclear factor-kappaB activation.Expression of the serum- and glucocorticoid-inducible protein kinase, Sgk, is a cell survival response to multiple types of environmental stress stimuli in mammary epithelial cells.Intracellular signalling mechanisms regulating glucose transport in insulin-sensitive tissues (review).Role of microvillar cell surfaces in the regulation of glucose uptake and organization of energy metabolism.JunD and JunB integrate prostaglandin E2 activation of breast cancer-associated proximal aromatase promoters.Regulation of the activity of p38 mitogen-activated protein kinase by Akt in cancer and adenoviral protein E1A-mediated sensitization to apoptosis.Transcriptional regulation of gene expression during osmotic stress responses by the mammalian target of rapamycin.Streptolysin S Promotes Programmed Cell Death and Enhances Inflammatory Signaling in Epithelial Keratinocytes during Group A Streptococcus Infection.Systematic study of cis-antisense miRNAs in animal species reveals miR-3661 to target PPP2CA in human cellsNLK phosphorylates Raptor to mediate stress-induced mTORC1 inhibition.Transcriptional regulation of the stress response by mTOR.Lysosomal recruitment of TSC2 is a universal response to cellular stressTSC2 mediates hyperosmotic stress-induced inactivation of mTORC1.The TORC1-activated Proteins, p70S6K and GRB10, Regulate IL-4 Signaling and M2 Macrophage Polarization by Modulating Phosphorylation of Insulin Receptor Substrate-2.Mechanism of activation of PKB/Akt by the protein phosphatase inhibitor Calyculin A.Antiapoptotic activity of Akt is down-regulated by Ca2+ in myocardiac H9c2 cells. Evidence of Ca(2+)-dependent regulation of protein phosphatase 2Ac.Signaling effects of demethylasterriquinone B1, a selective insulin receptor modulator.Overexpression of calreticulin modulates protein kinase B/Akt signaling to promote apoptosis during cardiac differentiation of cardiomyoblast H9c2 cells.Hyperosmolarity reduces GLUT4 endocytosis and increases its exocytosis from a VAMP2-independent pool in l6 muscle cells.Betaine improves nonalcoholic fatty liver and associated hepatic insulin resistance: a potential mechanism for hepatoprotection by betaine.Osmotic regulation of insulin-induced mitogen-activated protein kinase phosphatase (MKP-1) expression in H4IIE rat hepatoma cells.Arsenite stimulated glucose transport in 3T3-L1 adipocytes involves both Glut4 translocation and p38 MAPK activity.The trimeric GTP-binding protein (G(q)/G(11)) alpha subunit is required for insulin-stimulated GLUT4 translocation in 3T3L1 adipocytes.MKK6/3 and p38 MAPK pathway activation is not necessary for insulin-induced glucose uptake but regulates glucose transporter expression.A Crk-II/TC10 signaling pathway is required for osmotic shock-stimulated glucose transport.Volume-sensitive outwardly rectifying chloride channel in white adipocytes from normal and diabetic mice.Transactivation of ErbB2 and ErbB3 by tumor necrosis factor-alpha and anisomycin leads to impaired insulin signaling through serine/threonine phosphorylation of IRS proteins.NKCC activity restores muscle water during hyperosmotic challenge independent of insulin, ERK, and p38 MAPK.Protein phosphatase 2A-linked and -unlinked caspase-dependent pathways for downregulation of Akt kinase triggered by 4-hydroxynonenal.Protein kinase C-mediated down-regulation of cyclin D1 involves activation of the translational repressor 4E-BP1 via a phosphoinositide 3-kinase/Akt-independent, protein phosphatase 2A-dependent mechanism in intestinal epithelial cells.The impact of phosphatases on proliferative and survival signaling in cancer.
P2860
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P2860
Osmotic shock inhibits insulin signaling by maintaining Akt/protein kinase B in an inactive dephosphorylated state
description
1999 nî lūn-bûn
@nan
1999 թուականի Յուլիսին հրատարակուած գիտական յօդուած
@hyw
1999 թվականի հուլիսին հրատարակված գիտական հոդված
@hy
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
name
Osmotic shock inhibits insulin ...... nactive dephosphorylated state
@ast
Osmotic shock inhibits insulin ...... nactive dephosphorylated state
@en
type
label
Osmotic shock inhibits insulin ...... nactive dephosphorylated state
@ast
Osmotic shock inhibits insulin ...... nactive dephosphorylated state
@en
prefLabel
Osmotic shock inhibits insulin ...... nactive dephosphorylated state
@ast
Osmotic shock inhibits insulin ...... nactive dephosphorylated state
@en
P2093
P2860
P356
P1476
Osmotic shock inhibits insulin ...... nactive dephosphorylated state
@en
P2093
P2860
P304
P356
10.1128/MCB.19.7.4684
P407
P577
1999-07-01T00:00:00Z