An obligatory requirement for the heterotrimeric G protein Gi3 in the antiautophagic action of insulin in the liver. - Wikidata - awgldk - TriplyDB

An obligatory requirement for the heterotrimeric G protein Gi3 in the antiautophagic action of insulin in the liver.

An obligatory requirement for the heterotrimeric G protein Gi3 in the antiautophagic action of insulin in the liver.

http://www.wikidata.org/entity/Q35669855

about

Regulator of G-protein signaling 19 (RGS19) and its partner Gα-inhibiting activity polypeptide 3 (GNAI3) are required for zVAD-induced autophagy and cell death in L929 cells LAMP-2 is required for incorporating syntaxin-17 into autophagosomes and for their fusion with lysosomes.Biochemical isolation and characterization of the tubulovesicular LC3-positive autophagosomal compartment.Canonical and noncanonical g-protein signaling helps coordinate actin dynamics to promote macrophage phagocytosis of zymosan Defective Gpsm2/Gαi3 signalling disrupts stereocilia development and growth cone actin dynamics in Chudley-McCullough syndrome Transcription factor Emx2 controls stereociliary bundle orientation of sensory hair cells.Gαi2- and Gαi3-deficient mice display opposite severity of myocardial ischemia reperfusion injury Distribution of activator of G-protein signaling 3 within the aggresomal pathway: role of specific residues in the tetratricopeptide repeat domain and differential regulation by the AGS3 binding partners Gi(alpha) and mammalian inscuteable.Modulation of alpha2-adrenoceptor functions by heterotrimeric Galphai protein isoforms G protein-coupled receptors and the regulation of autophagy.Involvement of OA1, an intracellular GPCR, and G alpha i3, its binding protein, in melanosomal biogenesis and optic pathway formation Implications of non-canonical G-protein signaling for the immune system Variations in Gnai2 and Rgs1 expression affect chemokine receptor signaling and the organization of secondary lymphoid organs.Specific interaction of Gαi3 with the Oa1 G-protein coupled receptor controls the size and density of melanosomes in retinal pigment epithelium.Gαi2- and Gαi3-specific regulation of voltage-dependent L-type calcium channels in cardiomyocytes.Galpha(i1) and Galpha(i3) are required for epidermal growth factor-mediated activation of the Akt-mTORC1 pathway Augmented glucose-induced insulin release in mice lacking G(o2), but not G(o1) or G(i) proteins A GDI (AGS3) and a GEF (GIV) regulate autophagy by balancing G protein activity and growth factor signals Normal autophagic activity in macrophages from mice lacking Gαi3, AGS3, or RGS19.Roles of the 15-kDa selenoprotein (Sep15) in redox homeostasis and cataract development revealed by the analysis of Sep 15 knockout mice Platelet Gi protein Gαi2 is an essential mediator of thrombo-inflammatory organ damage in mice.The role of inhibitory heterotrimeric G proteins in the control of in vivo heart rate dynamics.Absence of the inhibitory G-protein Galphai2 predisposes to ventricular cardiac arrhythmia.Lack of Gαi2 leads to dilative cardiomyopathy and increased mortality in β1-adrenoceptor overexpressing mice Development of the mammalian axial skeleton requires signaling through the Gα(i) subfamily of heterotrimeric G proteins.Requirement of Galphai in thymic homing and early T cell development.Functions of autophagy in normal and diseased liver.Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use in investigating mechanisms of hepatotoxicity, cell signaling and ADME.Autophagy in the liver.Autophagic disposal of the aggregation-prone protein that causes liver inflammation and carcinogenesis in alpha-1-antitrypsin deficiency.G protein γ subunit 7 induces autophagy and inhibits cell division.Autophagy: regulation and role in disease.G(i)α proteins exhibit functional differences in the activation of ERK1/2, Akt and mTORC1 by growth factors in normal and breast cancer cells.α1-antitrypsin Deficiency: A Misfolded Secretory Protein Variant with Unique Effects on the Endoplasmic Reticulum.Hepatic fibrosis and carcinogenesis in α1-antitrypsin deficiency: a prototype for chronic tissue damage in gain-of-function disorders.Novel treatment strategies for liver disease due to α1-antitrypsin deficiency.Anti-nociceptive action of peripheral mu-opioid receptors by G-beta-gamma protein-mediated inhibition of TRPM3 channels.The impact of RGS and other G-protein regulatory proteins on Gαi-mediated signaling in immunity.Regulation, Signaling, and Physiological Functions of G-Proteins.AIP inactivation leads to pituitary tumorigenesis through defective Gαi-cAMP signaling.

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An obligatory requirement for the heterotrimeric G protein Gi3 in the antiautophagic action of insulin in the liver.

http://www.wikidata.org/entity/Q35669855

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2007 nî lūn-bûn

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Proceedings of the National Academy of Sciences of the United States of America

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Antje Gohla

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Bernd Nürnberg

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Dieter Häussinger

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Karinna Klement

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Karsten Spicher

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Katja Pexa

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Lutz Birnbaumer

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Roland P Piekorz

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Stephan vom Dahl

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Vladyslav Dreval

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P2860

Identification and characterization of GIV, a novel Galpha i/s-interacting protein found on COPI, endoplasmic reticulum-Golgi transport vesicles

LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing

Differential distribution of alpha subunits and beta gamma subunits of heterotrimeric G proteins on Golgi membranes of the exocrine pancreas

Heterotrimeric G protein subunits are located on rat liver endosomes

TOR signaling in growth and metabolism

Induction of autophagy and inhibition of tumorigenesis by beclin 1

Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice

Loss of autophagy in the central nervous system causes neurodegeneration in mice

GAIP, GIPC and Galphai3 are concentrated in endocytic compartments of proximal tubule cells: putative role in regulating megalin's function

LC3 conjugation system in mammalian autophagy

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104

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17296938

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1815296

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