Mitochondrial complex I activity and NAD+/NADH balance regulate breast cancer progression. - Wikidata - awgldk - TriplyDB

Mitochondrial complex I activity and NAD+/NADH balance regulate breast cancer progression.

Mitochondrial complex I activity and NAD+/NADH balance regulate breast cancer progression.

http://www.wikidata.org/entity/Q36638143

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Identification of druggable cancer driver genes amplified across TCGA datasets Emerging therapeutic roles for NAD(+) metabolism in mitochondrial and age-related disorders Hyperglycemic Stress and Carbon Stress in Diabetic Glucotoxicity Cancer metabolism and oxidative stress: Insights into carcinogenesis and chemotherapy via the non-dihydrofolate reductase effects of methotrexate Breast Cancer Metabolism and Mitochondrial Activity: The Possibility of Chemoprevention with Metformin Role of lipid peroxidation derived 4-hydroxynonenal (4-HNE) in cancer: focusing on mitochondria Redox control of glutamine utilization in cancer The mitochondrial permeability transition pore and cancer: molecular mechanisms involved in cell death Modulation of tumorigenesis by dietary intervention is not mediated by SIRT1 catalytic activity Resveratrol Directly Binds to Mitochondrial Complex I and Increases Oxidative Stress in Brain Mitochondria of Aged Mice Sources and implications of NADH/NAD(+) redox imbalance in diabetes and its complications Causes of genome instability: the effect of low dose chemical exposures in modern society Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead Reduced Warburg effect in cancer cells undergoing autophagy: steady- state 1H-MRS and real-time hyperpolarized 13C-MRS studies Prioritizing protein complexes implicated in human diseases by network optimization Simultaneous Analysis of Major Coenzymes of Cellular Redox Reactions and Energy Using ex Vivo (1)H NMR Spectroscopy Tumor microenvironment derived exosomes pleiotropically modulate cancer cell metabolism The use of EEM fluorescence data and OPLS/UPLS-DA algorithm to discriminate between normal and cancer cell lines: a feasibility study.An integer programming framework for inferring disease complexes from network data.mtDNA, Metastasis, and the Mitochondrial Unfolded Protein Response (UPRmt).Oxidation of alpha-ketoglutarate is required for reductive carboxylation in cancer cells with mitochondrial defects.Uncoupling genotoxic stress responses from circadian control increases susceptibility to mammary carcinogenesis.Putative role of adipose tissue in growth and metabolism of colon cancer cells.Coexpression within Integrated Mitochondrial Pathways Reveals Different Networks in Normal and Chemically Treated Transcriptomes.Dichloroacetate induces autophagy in colorectal cancer cells and tumours.Breast cancer stem cells rely on fermentative glycolysis and are sensitive to 2-deoxyglucose treatment.Essential role of TID1 in maintaining mitochondrial membrane potential homogeneity and mitochondrial DNA integrity.Metabolic determinants of cancer cell sensitivity to glucose limitation and biguanides.Metabolic reprogramming and dysregulated metabolism: cause, consequence and/or enabler of environmental carcinogenesis?Nicotinamide phosphoribosyltransferase can affect metastatic activity and cell adhesive functions by regulating integrins in breast cancer.Nicotinamide phosphoribosyltransferase promotes epithelial-to-mesenchymal transition as a soluble factor independent of its enzymatic activity FTSJ2, a heat shock-inducible mitochondrial protein, suppresses cell invasion and migration.The vitamin D receptor inhibits the respiratory chain, contributing to the metabolic switch that is essential for cancer cell proliferation.Cell-permeable protein therapy for complex I dysfunction Focal adhesion kinase-promoted tumor glucose metabolism is associated with a shift of mitochondrial respiration to glycolysis.Down-Regulation of NDUFB9 Promotes Breast Cancer Cell Proliferation, Metastasis by Mediating Mitochondrial Metabolism.An Essential Role of the Mitochondrial Electron Transport Chain in Cell Proliferation Is to Enable Aspartate Synthesis Effects of Selenium Yeast on Oxidative Stress, Growth Inhibition, and Apoptosis in Human Breast Cancer Cells.Metabolic Plasticity in Cancer Cells: Reconnecting Mitochondrial Function to Cancer Control.Male-specific association between MT-ND4 11719 A/G polymorphism and ulcerative colitis: a mitochondria-wide genetic association study

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P2860

Mitochondrial complex I activity and NAD+/NADH balance regulate breast cancer progression.

http://www.wikidata.org/entity/Q36638143

description

2013 nî lūn-bûn

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年论文

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2013年论文

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2013年论文

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name

Mitochondrial complex I activi ...... ate breast cancer progression.

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Mitochondrial complex I activi ...... ate breast cancer progression.

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type

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Mitochondrial complex I activi ...... ate breast cancer progression.

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Mitochondrial complex I activi ...... ate breast cancer progression.

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Mitochondrial complex I activi ...... ate breast cancer progression.

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Mitochondrial complex I activi ...... ate breast cancer progression.

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Journal of Clinical Investigation

P1476

Mitochondrial complex I activity and NAD+/NADH balance regulate breast cancer progression

@en

P2093

Akemi Matsuno-Yagi

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Antonio F Santidrian

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Brunhilde Felding-Habermann

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Byoung B Seo

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Laurie J Gay

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Melissa Ritland

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Takao Yagi

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P2860

SIRT1 negatively regulates the mammalian target of rapamycin

Cancer as an evolutionary and ecological process

Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes

Transcriptional regulation of BRCA1 expression by a metabolic switch

A role for the NAD-dependent deacetylase Sirt1 in the regulation of autophagy

SIRT1 modulation of the acetylation status, cytosolic localization, and activity of LKB1. Possible role in AMP-activated protein kinase activation

Understanding the Warburg effect: the metabolic requirements of cell proliferation

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

Autophagy suppresses tumorigenesis through elimination of p62

Mitochondrial defects in cancer

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1068-1081

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10.1172/JCI64264

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3

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123

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Sarah E LeBoeuf

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23426180

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3582128

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