Glucose addiction of TSC null cells is caused by failed mTORC1-dependent balancing of metabolic demand with supply. - Wikidata - wikimedia - TriplyDB

Glucose addiction of TSC null cells is caused by failed mTORC1-dependent balancing of metabolic demand with supply.

Glucose addiction of TSC null cells is caused by failed mTORC1-dependent balancing of metabolic demand with supply.

http://www.wikidata.org/entity/Q42069435

about

Mammalian target of rapamycin up-regulation of pyruvate kinase isoenzyme type M2 is critical for aerobic glycolysis and tumor growth Osmotic stress regulates mammalian target of rapamycin (mTOR) complex 1 via c-Jun N-terminal Kinase (JNK)-mediated Raptor protein phosphorylation Lactate Contribution to the Tumor Microenvironment: Mechanisms, Effects on Immune Cells and Therapeutic Relevance mTOR-dependent cell survival mechanisms Therapeutic targeting of cellular metabolism in cells with hyperactive mTORC1: a paradigm shift Novel therapeutic targets of tumor metabolism Glutamine and cancer: cell biology, physiology, and clinical opportunities Appetite for destruction: the inhibition of glycolysis as a therapy for tuberous sclerosis complex-related tumors Nutrient sensing, metabolism, and cell growth control Nutrient regulation of the mTOR complex 1 signaling pathway Real-time monitoring of tumorigenesis, dissemination, & drug response in a preclinical model of lymphangioleiomyomatosis/tuberous sclerosis complex Green Tea Polyphenols Control Dysregulated Glutamate Dehydrogenase in Transgenic Mice by Hijacking the ADP Activation Site mTOR drives its own activation via SCF(βTrCP)-dependent degradation of the mTOR inhibitor DEPTOR Tsc1 (hamartin) confers neuroprotection against ischemia by inducing autophagy The eEF2 kinase confers resistance to nutrient deprivation by blocking translation elongation The mTORC1 pathway stimulates glutamine metabolism and cell proliferation by repressing SIRT4 SIRT4 has tumor-suppressive activity and regulates the cellular metabolic response to DNA damage by inhibiting mitochondrial glutamine metabolism ROS signaling under metabolic stress: cross-talk between AMPK and AKT pathway.Critical role of SCD1 in autophagy regulation via lipogenesis and lipid rafts-coupled AKT-FOXO1 signaling pathway.Current views on cell metabolism in SDHx-related pheochromocytoma and paraganglioma The glutamate/cystine xCT antiporter antagonizes glutamine metabolism and reduces nutrient flexibility.Autophagy-dependent metabolic reprogramming sensitizes TSC2-deficient cells to the antimetabolite 6-aminonicotinamide Estradiol promotes pentose phosphate pathway addiction and cell survival via reactivation of Akt in mTORC1 hyperactive cells.mTORC1-Driven Tumor Cells Are Highly Sensitive to Therapeutic Targeting by Antagonists of Oxidative Stress.Hepatic mTORC1 controls locomotor activity, body temperature, and lipid metabolism through FGF21.Tumor bioenergetics: an emerging avenue for cancer metabolism targeted therapy Tumorigenesis in tuberous sclerosis complex is autophagy and p62/sequestosome 1 (SQSTM1)-dependent.LKB1 is a central regulator of tumor initiation and pro-growth metabolism in ErbB2-mediated breast cancer.Evolving Lessons on the Complex Role of AMPK in Normal Physiology and Cancer.A cell-autonomous molecular cascade initiated by AMP-activated protein kinase represses steroidogenesis Synthetic lethality of combined glutaminase and Hsp90 inhibition in mTORC1-driven tumor cells Pyruvate carboxylase is required for glutamine-independent growth of tumor cells.Mammalian target of rapamycin complex I (mTORC1) activity in ras homologue enriched in brain (Rheb)-deficient mouse embryonic fibroblasts Phospholipase D mediates nutrient input to mammalian target of rapamycin complex 1 (mTORC1).Hyperactivated Wnt signaling induces synthetic lethal interaction with Rb inactivation by elevating TORC1 activities.The tumor suppressor Tsc1 enforces quiescence of naive T cells to promote immune homeostasis and function.The multikinase inhibitor Sorafenib enhances glycolysis and synergizes with glycolysis blockade for cancer cell killing.Phosphoproteomic analysis identifies Grb10 as an mTORC1 substrate that negatively regulates insulin signaling.Activated mTORC1 promotes long-term cone survival in retinitis pigmentosa mice.Glucose deprivation in tuberous sclerosis complex-related tumors.

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Glucose addiction of TSC null cells is caused by failed mTORC1-dependent balancing of metabolic demand with supply.

http://www.wikidata.org/entity/Q42069435

description

2010 nî lūn-bûn

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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2010年论文

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2010年论文

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name

Glucose addiction of TSC null ...... metabolic demand with supply.

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Glucose addiction of TSC null ...... metabolic demand with supply.

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type

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Glucose addiction of TSC null ...... metabolic demand with supply.

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Glucose addiction of TSC null ...... metabolic demand with supply.

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prefLabel

Glucose addiction of TSC null ...... metabolic demand with supply.

@en

Glucose addiction of TSC null ...... metabolic demand with supply.

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Glucose addiction of TSC null ...... metabolic demand with supply.

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Andrew Y Choo

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

Hieu Vu

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

John Blenis

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

Lewis C Cantley

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

Matthew G Vander Heiden

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

Sang Gyun Kim

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

Sang-Oh Yoon

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Sarah J Mahoney

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P2860

AMPK phosphorylation of raptor mediates a metabolic checkpoint

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

TSC2 mediates cellular energy response to control cell growth and survival

Rag proteins regulate amino-acid-induced mTORC1 signalling.

Growth factor regulation of autophagy and cell survival in the absence of apoptosis

The transcription factor HIF-1alpha plays a critical role in the growth factor-dependent regulation of both aerobic and anaerobic glycolysis

The biology of cancer: metabolic reprogramming fuels cell growth and proliferation

Ras, PI(3)K and mTOR signalling controls tumour cell growth

Molecular mechanisms of mTOR-mediated translational control

Myc regulates a transcriptional program that stimulates mitochondrial glutaminolysis and leads to glutamine addiction

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