Hepatic mTORC2 activates glycolysis and lipogenesis through Akt, glucokinase, and SREBP1c. - Wikidata - awgldk - TriplyDB

Hepatic mTORC2 activates glycolysis and lipogenesis through Akt, glucokinase, and SREBP1c.

Hepatic mTORC2 activates glycolysis and lipogenesis through Akt, glucokinase, and SREBP1c.

http://www.wikidata.org/entity/Q34269920

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Nonalcoholic fatty liver disease: a comprehensive review of a growing epidemic Feature Article: mTOR complex 2-Akt signaling at mitochondria-associated endoplasmic reticulum membranes (MAM) regulates mitochondrial physiology Regulation of liver development: implications for liver biology across the lifespan Transcriptional regulation of hepatic lipogenesis Energy metabolism in the liver The genetic and epigenetic alterations in human hepatocellular carcinoma: a recent update The combined hyperlipidemia caused by impaired Wnt-LRP6 signaling is reversed by Wnt3a rescue mTOR and differential activation of mitochondria orchestrate neutrophil chemotaxis PGC-1/Spargel Counteracts High-Fat-Diet-Induced Obesity and Cardiac Lipotoxicity Downstream of TOR and Brummer ATGL Lipase.Judicious Toggling of mTOR Activity to Combat Insulin Resistance and Cancer: Current Evidence and Perspectives mTOR activation is a biomarker and a central pathway to autoimmune disorders, cancer, obesity, and aging Depletion of Rictor, an essential protein component of mTORC2, decreases male lifespan The Mechanistic Target of Rapamycin: The Grand ConducTOR of Metabolism and Aging Hepatic signaling by the mechanistic target of rapamycin complex 2 (mTORC2)Where is mTOR and what is it doing there?Sestrin 3 protein enhances hepatic insulin sensitivity by direct activation of the mTORC2-Akt signaling The Complex Roles of Mechanistic Target of Rapamycin in Adipocytes and Beyond.Acid sphingomyelinase deficiency in Western diet-fed mice protects against adipocyte hypertrophy and diet-induced liver steatosis.Increased glucose metabolism and alpha-glucosidase inhibition in Cordyceps militaris water extract-treated HepG2 cells.Rictor/mTORC2 facilitates central regulation of energy and glucose homeostasis.mTORC2 in the center of cancer metabolic reprogramming Insulin signaling, resistance, and the metabolic syndrome: insights from mouse models into disease mechanisms.Akt phosphorylation and regulation of transketolase is a nodal point for amino acid control of purine synthesis Mechanistic target of rapamycin complex 2 protects the heart from ischemic damage Acute mTOR inhibition induces insulin resistance and alters substrate utilization in vivo Liver clock protein BMAL1 promotes de novo lipogenesis through insulin-mTORC2-AKT signaling In vivo evidence for mTORC2-mediated actin cytoskeleton rearrangement in neurons The adaptor protein p66Shc inhibits mTOR-dependent anabolic metabolism.Glycogen phosphorylase inhibitor N-(3,5-dimethyl-Benzoyl)-N'-(β-D-glucopyranosyl)urea improves glucose tolerance under normoglycemic and diabetic conditions and rearranges hepatic metabolism.Emerging function of mTORC2 as a core regulator in glioblastoma: metabolic reprogramming and drug resistance.Restriction on an energy-dense diet improves markers of metabolic health and cellular aging in mice through decreasing hepatic mTOR activity C-C chemokine receptor 2 inhibitor ameliorates hepatic steatosis by improving ER stress and inflammation in a type 2 diabetic mouse model.mTORC2 regulates renal tubule sodium uptake by promoting ENaC activity.TGFβ-induced deptor suppression recruits mTORC1 and not mTORC2 to enhance collagen I (α2) gene expression.Conditional disruption of rictor demonstrates a direct requirement for mTORC2 in skin tumor development and continued growth of established tumors mTOR and metabolic regulation of conventional and regulatory T cells.Livers with constitutive mTORC1 activity resist steatosis independent of feedback suppression of Akt.Synergistic Effects between mTOR Complex 1/2 and Glycolysis Inhibitors in Non-Small-Cell Lung Carcinoma Cells.Chronic Mild Cold Conditioning Modulates the Expression of Hypothalamic Neuropeptide and Intermediary Metabolic-Related Genes and Improves Growth Performances in Young Chicks Once again on rapamycin-induced insulin resistance and longevity: despite of or owing to.

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Hepatic mTORC2 activates glycolysis and lipogenesis through Akt, glucokinase, and SREBP1c.

http://www.wikidata.org/entity/Q34269920

description

2012 nî lūn-bûn

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2012 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2012 թվականի ապրիլին հրատարակված գիտական հոդված

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年论文

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name

Hepatic mTORC2 activates glyco ...... Akt, glucokinase, and SREBP1c.

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Hepatic mTORC2 activates glyco ...... Akt, glucokinase, and SREBP1c.

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Hepatic mTORC2 activates glyco ...... Akt, glucokinase, and SREBP1c.

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type

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Hepatic mTORC2 activates glyco ...... Akt, glucokinase, and SREBP1c.

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Hepatic mTORC2 activates glyco ...... Akt, glucokinase, and SREBP1c.

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Hepatic mTORC2 activates glyco ...... Akt, glucokinase, and SREBP1c.

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Hepatic mTORC2 activates glyco ...... Akt, glucokinase, and SREBP1c.

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Hepatic mTORC2 activates glyco ...... Akt, glucokinase, and SREBP1c.

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Hepatic mTORC2 activates glyco ...... Akt, glucokinase, and SREBP1c.

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J.CMET.2012.03.015

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Cell Metabolism

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Hepatic mTORC2 activates glyco ...... Akt, glucokinase, and SREBP1c.

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Asami Hagiwara

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Francesca Trapani

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Luigi Terracciano

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Marion Cornu

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Markus A Rüegg

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Michael N Hall

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Nadine Cybulski

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Pazit Polak

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725-738

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scholarly article

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10.1016/J.CMET.2012.03.015

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5

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15

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224810417

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22521878

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