The glucose dependence of Akt-transformed cells can be reversed by pharmacologic activation of fatty acid beta-oxidation. - Wikidata - awgldk - TriplyDB

The glucose dependence of Akt-transformed cells can be reversed by pharmacologic activation of fatty acid beta-oxidation.

The glucose dependence of Akt-transformed cells can be reversed by pharmacologic activation of fatty acid beta-oxidation.

http://www.wikidata.org/entity/Q46418283

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Shikonin directly targets mitochondria and causes mitochondrial dysfunction in cancer cells.Understanding the Warburg effect: the metabolic requirements of cell proliferation Expression of transketolase TKTL1 predicts colon and urothelial cancer patient survival: Warburg effect reinterpreted Brick by brick: metabolism and tumor cell growth Novel drugs that target the metabolic reprogramming in renal cell cancer MicroRNA in Metabolic Re-Programming and Their Role in Tumorigenesis Mitochondrial Dysfunction in Cancer and Neurodegenerative Diseases: Spotlight on Fatty Acid Oxidation and Lipoperoxidation Products Starved and Asphyxiated: How Can CD8(+) T Cells within a Tumor Microenvironment Prevent Tumor Progression AMPK as a potential anticancer target - friend or foe?Molecular biology of gliomas: present and future challenges Autophagy: a targetable linchpin of cancer cell metabolism Drugging the addict: non-oncogene addiction as a target for cancer therapy Regulation and function of proline oxidase under nutrient stress The eEF2 kinase confers resistance to nutrient deprivation by blocking translation elongation Progress and prospects of reactive oxygen species in metal carcinogenesis SIRT3 and cancer: tumor promoter or suppressor?Differentially expressed proteins in malignant and benign adrenocortical tumors Activation of β-catenin by oncogenic PIK3CA and EGFR promotes resistance to glucose deprivation by inducing a strong antioxidant response Isoorientin induces apoptosis, decreases invasiveness, and downregulates VEGF secretion by activating AMPK signaling in pancreatic cancer cells The LKB1-AMPK pathway: metabolism and growth control in tumour suppression Metabolic reprogramming: a cancer hallmark even warburg did not anticipate The genomic analysis of lactic acidosis and acidosis response in human cancers Oxygen consumption can regulate the growth of tumors, a new perspective on the Warburg effect.Metabolic profiling reveals key metabolic features of renal cell carcinoma.Enhancing CD8 T-cell memory by modulating fatty acid metabolism The glutamate/cystine xCT antiporter antagonizes glutamine metabolism and reduces nutrient flexibility.Coordinated metabolic transitions during Drosophila embryogenesis and the onset of aerobic glycolysis.Akt and c-Myc differentially activate cellular metabolic programs and prime cells to bioenergetic inhibition.Monoacylglycerol lipase regulates a fatty acid network that promotes cancer pathogenesis.Modulation of glucose transporter 1 (GLUT1) expression levels alters mouse mammary tumor cell growth in vitro and in vivo.Targeting bioenergetics to enhance cancer chemotherapy: mitochondria SLP into apoptosis.Memory CD8(+) T cells use cell-intrinsic lipolysis to support the metabolic programming necessary for development.Antioxidant and oncogene rescue of metabolic defects caused by loss of matrix attachment Bone marrow fat: linking adipocyte-induced inflammation with skeletal metastases From genotype to functional phenotype: unraveling the metabolomic features of colorectal cancer.Upregulation of glucose metabolism by NF-κB2/p52 mediates enzalutamide resistance in castration-resistant prostate cancer cells.Metabolism and proliferation share common regulatory pathways in cancer cells.Multiple metabolic alterations exist in mutant PI3K cancers, but only glucose is essential as a nutrient source Inhibition of fatty acid metabolism reduces human myeloma cells proliferation.MUC1 oncoprotein promotes autophagy in a survival response to glucose deprivation.

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P2860

The glucose dependence of Akt-transformed cells can be reversed by pharmacologic activation of fatty acid beta-oxidation.

http://www.wikidata.org/entity/Q46418283

description

2005 nî lūn-bûn

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年學術文章

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2005年學術文章

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2005年學術文章

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name

The glucose dependence of Akt- ...... of fatty acid beta-oxidation.

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The glucose dependence of Akt- ...... of fatty acid beta-oxidation.

@nl

type

label

The glucose dependence of Akt- ...... of fatty acid beta-oxidation.

@en

The glucose dependence of Akt- ...... of fatty acid beta-oxidation.

@nl

prefLabel

The glucose dependence of Akt- ...... of fatty acid beta-oxidation.

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The glucose dependence of Akt- ...... of fatty acid beta-oxidation.

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The glucose dependence of Akt- ...... of fatty acid beta-oxidation.

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P2093

Craig B Thompson

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

Daniel E Bauer

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

Georgia Hatzivassiliou

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

Monica Buzzai

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

Ralph J Deberardinis

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

Rebecca L Elstrom

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Russell G Jones

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

P2860

TSC2 mediates cellular energy response to control cell growth and survival

A role for AMP-activated protein kinase in contraction- and hypoxia-regulated glucose transport in skeletal muscle

AMP-activated protein kinase suppresses protein synthesis in rat skeletal muscle through down-regulated mammalian target of rapamycin (mTOR) signaling

Activation of AMP-activated protein kinase leads to the phosphorylation of elongation factor 2 and an inhibition of protein synthesis

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

BAD and glucokinase reside in a mitochondrial complex that integrates glycolysis and apoptosis

5-aminoimidazole-4-carboxamide ribonucleoside. A specific method for activating AMP-activated protein kinase in intact cells?

Akt stimulates aerobic glycolysis in cancer cells

Oncogenic alterations of metabolism.

Glucose repression in yeast.

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10.1038/SJ.ONC.1208622

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26

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24

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15806154

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