The trimeric GTP-binding protein (G(q)/G(11)) alpha subunit is required for insulin-stimulated GLUT4 translocation in 3T3L1 adipocytes. (Q42484509)

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4 November 2019

title

The trimeric GTP-binding protein (G(q)/G(11)) alpha subunit is required for insulin-stimulated GLUT4 translocation in 3T3L1 adipocytes (English)

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4 November 2019

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4 November 2019

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4 November 2019

R T Watson

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4 November 2019

J E Pessin

series ordinal

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4 November 2019

language of work or name

English

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publication date

1 March 2000

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Journal of Biological Chemistry

4 November 2019

published in

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4 November 2019

volume

275

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4 November 2019

issue

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4 November 2019

page(s)

7167-7175

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Structure, function, and regulation of the mammalian facilitative glucose transporter gene family

4 November 2019

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Inhibition of the translocation of GLUT1 and GLUT4 in 3T3-L1 cells by the phosphatidylinositol 3-kinase inhibitor, wortmannin

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Overexpression of catalytic subunit p110alpha of phosphatidylinositol 3-kinase increases glucose transport activity with translocation of glucose transporters in 3T3-L1 adipocytes

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Requirement for phosphoinositide 3-kinase in insulin-stimulated GLUT4 translocation in 3T3-L1 adipocytes

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Phosphatidylinositol 3-kinase activation is required for insulin stimulation of pp70 S6 kinase, DNA synthesis, and glucose transporter translocation

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Activated phosphatidylinositol 3-kinase is sufficient to mediate actin rearrangement and GLUT4 translocation in 3T3-L1 adipocytes

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Adenovirus-Mediated Overexpression of IRS-1 Interacting Domains Abolishes Insulin-Stimulated Mitogenesis without Affecting Glucose Transport in 3T3-L1 Adipocytes

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Okadaic acid activates atypical protein kinase C (zeta/lambda) in rat and 3T3/L1 adipocytes. An apparent requirement for activation of Glut4 translocation and glucose transport

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Protein kinase C isotypes controlled by phosphoinositide 3-kinase through the protein kinase PDK1

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Expression of a constitutively active Akt Ser/Thr kinase in 3T3-L1 adipocytes stimulates glucose uptake and glucose transporter 4 translocation

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Protein kinase B/Akt participates in GLUT4 translocation by insulin in L6 myoblasts

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Requirement for activation of the serine-threonine kinase Akt (protein kinase B) in insulin stimulation of protein synthesis but not of glucose transport

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Requirement of atypical protein kinase clambda for insulin stimulation of glucose uptake but not for Akt activation in 3T3-L1 adipocytes

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Activation of protein kinase C (alpha, beta, and zeta) by insulin in 3T3/L1 cells. Transfection studies suggest a role for PKC-zeta in glucose transport

21 January 2018

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Osmotic Shock Stimulates GLUT4 Translocation in 3T3L1 Adipocytes by a Novel Tyrosine Kinase Pathway

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Osmotic shock inhibits insulin signaling by maintaining Akt/protein kinase B in an inactive dephosphorylated state

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Bradykinin directly triggers GLUT4 translocation via an insulin-independent pathway.

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21 January 2018

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21 January 2018

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21 January 2018

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Regulation of insulin-stimulated glucose transporter GLUT4 translocation and Akt kinase activity by ceramide.

21 January 2018

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The inability of phosphatidylinositol 3-kinase activation to stimulate GLUT4 translocation indicates additional signaling pathways are required for insulin-stimulated glucose uptake

21 January 2018

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21 January 2018

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G alpha-q/11 protein plays a key role in insulin-induced glucose transport in 3T3-L1 adipocytes

21 January 2018

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