Regulation of mTORC1 by the Rag GTPases is necessary for neonatal autophagy and survival. - Wikidata - awgldk - TriplyDB

Regulation of mTORC1 by the Rag GTPases is necessary for neonatal autophagy and survival.

Regulation of mTORC1 by the Rag GTPases is necessary for neonatal autophagy and survival.

http://www.wikidata.org/entity/Q37725045

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Metabolism. Lysosomal amino acid transporter SLC38A9 signals arginine sufficiency to mTORC1 Conserved regulators of Rag GTPases orchestrate amino acid-dependent TORC1 signaling Advances in Autophagy Regulatory Mechanisms Regulation of liver development: implications for liver biology across the lifespan The neurology of mTOR Regulation of mTORC1 by PI3K signaling Nutrient-sensing mechanisms across evolution Regulation of mTORC1 by amino acids Reciprocal conversion of Gtr1 and Gtr2 nucleotide-binding states by Npr2-Npr3 inactivates TORC1 and induces autophagy.Nucleotide degradation and ribose salvage in yeast.SEACing the GAP that nEGOCiates TORC1 activation: evolutionary conservation of Rag GTPase regulation.Sestrins inhibit mTORC1 kinase activation through the GATOR complex The Sestrins interact with GATOR2 to negatively regulate the amino-acid-sensing pathway upstream of mTORC1 Sestrins function as guanine nucleotide dissociation inhibitors for Rag GTPases to control mTORC1 signaling mTOR signaling in tumorigenesis The Mechanistic Target of Rapamycin: The Grand ConducTOR of Metabolism and Aging KICSTOR recruits GATOR1 to the lysosome and is necessary for nutrients to regulate mTORC1 SZT2 dictates GATOR control of mTORC1 signalling.Loss of hepatic DEPTOR alters the metabolic transition to fasting Lysosomal adaptation: how the lysosome responds to external cues RagA, but not RagB, is essential for embryonic development and adult mice.The TORC1 inhibitors Nprl2 and Nprl3 mediate an adaptive response to amino-acid starvation in Drosophila.Pompe disease: from pathophysiology to therapy and back again Functional effects of a pathogenic mutation in Cereblon (CRBN) on the regulation of protein synthesis via the AMPK-mTOR cascade.Amino acid-induced impairment of insulin sensitivity in healthy and obese rats is reversible.Signals from the lysosome: a control centre for cellular clearance and energy metabolism.Regulation of mTORC1 and its impact on gene expression at a glance.Role of autophagy in differential sensitivity of hepatocarcinoma cells to sorafenib.Acinus integrates AKT1 and subapoptotic caspase activities to regulate basal autophagy.Metabolic control of autophagy Diminished mTOR signaling: a common mode of action for endocrine longevity factors.Intersection of mTOR and STAT signaling in immunity Regulation of autophagy by mTOR-dependent and mTOR-independent pathways: autophagy dysfunction in neurodegenerative diseases and therapeutic application of autophagy enhancers.Nutrient-sensing mechanisms and pathways.Reduced autophagy in livers of fasted, fat-depleted, ghrelin-deficient mice: reversal by growth hormone.Regulation of autophagy via PERK-eIF2α effectively relieve the radiation myelitis induced by iodine-125 Transcriptional network analysis reveals that AT1 and AT2 angiotensin II receptors are both involved in the regulation of genes essential for glioma progression.Stress granule-defective mutants deregulate stress responsive transcripts.Defects in calcium homeostasis and mitochondria can be reversed in Pompe disease.Cordycepin induced MA-10 mouse Leydig tumor cell apoptosis by regulating p38 MAPKs and PI3K/AKT signaling pathways

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Regulation of mTORC1 by the Rag GTPases is necessary for neonatal autophagy and survival.

http://www.wikidata.org/entity/Q37725045

description

article científic

@ca

article scientifique

@fr

articolo scientifico

@it

artigo científico

@pt

bilimsel makale

@tr

scientific article published on 23 December 2012

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

Regulation of mTORC1 by the Rag GTPases is necessary for neonatal autophagy and survival.

@en

Regulation of mTORC1 by the Rag GTPases is necessary for neonatal autophagy and survival.

@nl

type

label

Regulation of mTORC1 by the Rag GTPases is necessary for neonatal autophagy and survival.

@en

Regulation of mTORC1 by the Rag GTPases is necessary for neonatal autophagy and survival.

@nl

prefLabel

Regulation of mTORC1 by the Rag GTPases is necessary for neonatal autophagy and survival.

@en

Regulation of mTORC1 by the Rag GTPases is necessary for neonatal autophagy and survival.

@nl

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Regulation of mTORC1 by the Rag GTPases is necessary for neonatal autophagy and survival

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David D Sabatini

http://www.w3.org/2001/XMLSchema#string

David M Sabatini

http://www.w3.org/2001/XMLSchema#string

Harriet Snitkin

http://www.w3.org/2001/XMLSchema#string

Iwona Gumper

http://www.w3.org/2001/XMLSchema#string

Rachel L Wolfson

http://www.w3.org/2001/XMLSchema#string

Roberto Zoncu

http://www.w3.org/2001/XMLSchema#string

Steven Chang

http://www.w3.org/2001/XMLSchema#string

P2860

Ragulator-Rag complex targets mTORC1 to the lysosomal surface and is necessary for its activation by amino acids

RagA is a functional homologue of S. cerevisiae Gtr1p involved in the Ran/Gsp1-GTPase pathway

The Rag GTPases bind raptor and mediate amino acid signaling to mTORC1

The tumor suppressor LKB1 kinase directly activates AMP-activated kinase and regulates apoptosis in response to energy stress

mTOR: from growth signal integration to cancer, diabetes and ageing

Autophagy fights disease through cellular self-digestion

Translational control is required for the unfolded protein response and in vivo glucose homeostasis

A mouse model of TSC1 reveals sex-dependent lethality from liver hemangiomas, and up-regulation of p70S6 kinase activity in Tsc1 null cells

Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice

Autophagy and the integrated stress response

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679-683

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scholarly article

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10.1038/NATURE11745

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7434

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493

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2012-12-23T00:00:00Z

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1020907837

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23263183

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4000705

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