Akt maintains cell size and survival by increasing mTOR-dependent nutrient uptake. - Wikidata - wikimedia - TriplyDB

Akt maintains cell size and survival by increasing mTOR-dependent nutrient uptake.

Akt maintains cell size and survival by increasing mTOR-dependent nutrient uptake.

http://www.wikidata.org/entity/Q39616081

about

SREBP activity is regulated by mTORC1 and contributes to Akt-dependent cell growth The insulin-like growth factor-I-mTOR signaling pathway induces the mitochondrial pyrimidine nucleotide carrier to promote cell growth Erk regulation of pyruvate dehydrogenase flux through PDK4 modulates cell proliferation Metabolic activation-related CD147-CD98 complex Brick by brick: metabolism and tumor cell growth AKT/PKB signaling: navigating downstream Controlling cell division in yeast and animals: does size matter?Novel drugs that target the metabolic reprogramming in renal cell cancer Metabolic, autophagic, and mitophagic activities in cancer initiation and progression Molecular Imaging of Metabolic Reprograming in Mutant IDH Cells Medical treatment for gastro-entero-pancreatic neuroendocrine tumours Metabolic regulation of T cell differentiation and function Rapalogs in cancer prevention: anti-aging or anticancer?Leucine and mTORC1: a complex relationship Autophagy: a targetable linchpin of cancer cell metabolism Role of AKT/mTORC1 pathway in pancreatic β-cell proliferation Metformin promotes tau aggregation and exacerbates abnormal behavior in a mouse model of tauopathy The Complexity of Targeting PI3K-Akt-mTOR Signalling in Human Acute Myeloid Leukaemia: The Importance of Leukemic Cell Heterogeneity, Neighbouring Mesenchymal Stem Cells and Immunocompetent Cells Adipose tissue dysfunction and its effects on tumor metabolism Feeding an army: The metabolism of T cells in activation, anergy, and exhaustion Nuclear targeting of 6-phosphofructo-2-kinase (PFKFB3) increases proliferation via cyclin-dependent kinases The PIM kinases in hematological cancers Phenethyl isothiocyanate exhibits antileukemic activity in vitro and in vivo by inactivation of Akt and activation of JNK pathways The serine/threonine kinase Pim-2 is a transcriptionally regulated apoptotic inhibitor RhoB controls Akt trafficking and stage-specific survival of endothelial cells during vascular development Nephrin and CD2AP associate with phosphoinositide 3-OH kinase and stimulate AKT-dependent signaling DNA damaging agents and p53 do not cause senescence in quiescent cells, while consecutive re-activation of mTOR is associated with conversion to senescence Genetic polymorphisms of mTOR and cancer risk: a systematic review and updated meta-analysis Bidirectional transport of amino acids regulates mTOR and autophagy Myc regulates a transcriptional program that stimulates mitochondrial glutaminolysis and leads to glutamine addiction Beyond aerobic glycolysis: transformed cells can engage in glutamine metabolism that exceeds the requirement for protein and nucleotide synthesis Rheb-TOR signaling promotes protein synthesis, but not glucose or amino acid import, in Drosophila Cluster analysis of protein array results via similarity of Gene Ontology annotation.Systems biology of lupus: mapping the impact of genomic and environmental factors on gene expression signatures, cellular signaling, metabolic pathways, hormonal and cytokine imbalance, and selecting targets for treatment.Glutamine metabolism is essential for human cytomegalovirus infection Mechanism of the salutary effects of estrogen on kupffer cell phagocytic capacity following trauma-hemorrhage: pivotal role of Akt activation.Causal reasoning identifies mechanisms of sensitivity for a novel AKT kinase inhibitor, GSK690693.T-cell and B-cell signaling biomarkers and treatment targets in lupus.Akt-dependent cell size regulation by the adhesion molecule on glia occurs independently of phosphatidylinositol 3-kinase and Rheb signaling.Akt and c-Myc differentially activate cellular metabolic programs and prime cells to bioenergetic inhibition.

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P2860

Akt maintains cell size and survival by increasing mTOR-dependent nutrient uptake.

http://www.wikidata.org/entity/Q39616081

description

2002 nî lūn-bûn

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2002年の論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年论文

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2002年论文

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2002年论文

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name

Akt maintains cell size and survival by increasing mTOR-dependent nutrient uptake.

@en

Akt maintains cell size and survival by increasing mTOR-dependent nutrient uptake.

@nl

type

label

Akt maintains cell size and survival by increasing mTOR-dependent nutrient uptake.

@en

Akt maintains cell size and survival by increasing mTOR-dependent nutrient uptake.

@nl

prefLabel

Akt maintains cell size and survival by increasing mTOR-dependent nutrient uptake.

@en

Akt maintains cell size and survival by increasing mTOR-dependent nutrient uptake.

@nl

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Molecular Biology of the Cell

P1476

Akt maintains cell size and survival by increasing mTOR-dependent nutrient uptake.

@en

P2093

Aimee L Edinger

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Craig B Thompson

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P2860

Growth factors can influence cell growth and survival through effects on glucose metabolism

Enhanced sensitivity of PTEN-deficient tumors to inhibition of FRAP/mTOR.

TOR, a central controller of cell growth.

A direct linkage between the phosphoinositide 3-kinase-AKT signaling pathway and the mammalian target of rapamycin in mitogen-stimulated and transformed cells

Oncogenic kinase signalling

Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo

Inhibition of early apoptotic events by Akt/PKB is dependent on the first committed step of glycolysis and mitochondrial hexokinase

Cellular survival: a play in three Akts

Evidence of insulin-stimulated phosphorylation and activation of the mammalian target of rapamycin mediated by a protein kinase B signaling pathway.

Differential sensitivity of various pediatric cancers and squamous cell carcinomas to lovastatin-induced apoptosis: therapeutic implications.

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2276-2288

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scholarly article

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10.1091/MBC.01-12-0584

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7

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13

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2002-07-01T00:00:00Z

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11247887

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12134068

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117312

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