K-ras(G12V) transformation leads to mitochondrial dysfunction and a metabolic switch from oxidative phosphorylation to glycolysis
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The Significance of Ras Activity in Pancreatic Cancer InitiationGenetics and biology of pancreatic ductal adenocarcinomaThe sweet trap in tumors: aerobic glycolysis and potential targets for therapyThe Warburg effect and drug resistanceComponents of cancer metabolism and therapeutic interventionsMitochondrial ROS in cancer: initiators, amplifiers or an Achilles' heel?Redox control of glutamine utilization in cancerIntracellular oxygen determined by respiration regulates localization of Ras and prenylated proteins.Changing perspective on oncometabolites: from metabolic signature of cancer to tumorigenic and immunosuppressive agentsArsenite-induced pseudo-hypoxia results in loss of anchorage-dependent growth in BEAS-2B pulmonary epithelial cellsSustained proliferation in cancer: Mechanisms and novel therapeutic targetsNovel role of NOX in supporting aerobic glycolysis in cancer cells with mitochondrial dysfunction and as a potential target for cancer therapyp53-mediated activation of the mitochondrial protease HtrA2/Omi prevents cell invasion.Induction of apoptosis by Cordyceps militaris fraction in human chronic myeloid leukemia K562 cells involved with mitochondrial dysfunction.Mutant KRas-Induced Mitochondrial Oxidative Stress in Acinar Cells Upregulates EGFR Signaling to Drive Formation of Pancreatic Precancerous Lesions.Mitochondrial dysfunction in some triple-negative breast cancer cell lines: role of mTOR pathway and therapeutic potentialActivating the expression of human K-rasG12D stimulates oncogenic transformation in transgenic goat fetal fibroblast cells.The vitamin D receptor inhibits the respiratory chain, contributing to the metabolic switch that is essential for cancer cell proliferation.Identification of NDUFAF1 in mediating K-Ras induced mitochondrial dysfunction by a proteomic screening approach.Deficient plastidic fatty acid synthesis triggers cell death by modulating mitochondrial reactive oxygen species.The Interplay between ROS and Ras GTPases: Physiological and Pathological Implications.A ROS-Activatable Agent Elicits Homologous Recombination DNA Repair and Synergizes with Pathway CompoundsClinical Severity of PGK1 Deficiency Due To a Novel p.E120K Substitution Is Exacerbated by Co-inheritance of a Subclinical Translocation t(3;14)(q26.33;q12), Disrupting NUBPL Gene.Cancer as a mitochondrial metabolic disease.Micro-RNA-155 is induced by K-Ras oncogenic signal and promotes ROS stress in pancreatic cancer.Oxidative Dimerization of PHD2 is Responsible for its Inactivation and Contributes to Metabolic Reprogramming via HIF-1α ActivationNovel oxidatively activated agents modify DNA and are enhanced by ercc1 silencing.Inhibition of glycolytic enzyme hexokinase II (HK2) suppresses lung tumor growth.Mitochondrial complex I activity and NAD+/NADH balance regulate breast cancer progression.Mutant Kras copy number defines metabolic reprogramming and therapeutic susceptibilitiesMitochondrial NDUFS3 regulates the ROS-mediated onset of metabolic switch in transformed cells.Hypoxic and Ras-transformed cells support growth by scavenging unsaturated fatty acids from lysophospholipids.Novel ROS-activated agents utilize a tethered amine to selectively target acute myeloid leukemia.Reolysin is a novel reovirus-based agent that induces endoplasmic reticular stress-mediated apoptosis in pancreatic cancer.RIP1 potentiates BPDE-induced transformation in human bronchial epithelial cells through catalase-mediated suppression of excessive reactive oxygen speciesFatty Acid Oxidation Mediated by Acyl-CoA Synthetase Long Chain 3 Is Required for Mutant KRAS Lung TumorigenesisDichloroacetate should be considered with platinum-based chemotherapy in hypoxic tumors rather than as a single agent in advanced non-small cell lung cancer.Cancer as a metabolic disease: implications for novel therapeutics.Metabolism addiction in pancreatic cancer.KRas, ROS and the initiation of pancreatic cancer
P2860
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P2860
K-ras(G12V) transformation leads to mitochondrial dysfunction and a metabolic switch from oxidative phosphorylation to glycolysis
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
2011年论文
@zh
2011年论文
@zh-cn
name
K-ras(G12V) transformation lea ...... phosphorylation to glycolysis
@ast
K-ras(G12V) transformation lea ...... phosphorylation to glycolysis
@en
type
label
K-ras(G12V) transformation lea ...... phosphorylation to glycolysis
@ast
K-ras(G12V) transformation lea ...... phosphorylation to glycolysis
@en
prefLabel
K-ras(G12V) transformation lea ...... phosphorylation to glycolysis
@ast
K-ras(G12V) transformation lea ...... phosphorylation to glycolysis
@en
P2093
P2860
P356
P1433
P1476
K-ras(G12V) transformation lea ...... phosphorylation to glycolysis
@en
P2093
Dunyaporn Trachootham
Helene Pelicano
Marcia Ogasawara
Paul J Chiao
Peng Huang
P2860
P2888
P304
P356
10.1038/CR.2011.145
P577
2011-08-30T00:00:00Z