Mitochondrial dysfunction contributes to oncogene-induced senescence. - Wikidata - wikimedia - TriplyDB

Mitochondrial dysfunction contributes to oncogene-induced senescence.

Mitochondrial dysfunction contributes to oncogene-induced senescence.

http://www.wikidata.org/entity/Q39837656

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Feedback between p21 and reactive oxygen production is necessary for cell senescence Cellular Senescence as the Causal Nexus of Aging Axis of ageing: telomeres, p53 and mitochondria Live imaging of innate immune cell sensing of transformed cells in zebrafish larvae: parallels between tumor initiation and wound inflammation Therapeutic Manipulation of Ageing: Repurposing Old Dogs and Discovering New Tricks Interplay between oxidant species and energy metabolism Novel role of NOX in supporting aerobic glycolysis in cancer cells with mitochondrial dysfunction and as a potential target for cancer therapy Glucocorticoids induce long-lasting effects in neural stem cells resulting in senescence-related alterations Protein kinase D1 is essential for Ras-induced senescence and tumor suppression by regulating senescence-associated inflammation.Iscador Qu inhibits doxorubicin-induced senescence of MCF7 cells Cellular senescence and protein degradation: breaking down cancer mTOR Signaling from Cellular Senescence to Organismal Aging Insulin-like growth factor-1 regulates the SIRT1-p53 pathway in cellular senescence.Impaired OXPHOS complex III in breast cancer Rejuvenating senescent and centenarian human cells by reprogramming through the pluripotent state.iPSCs as a major opportunity to understand and cure age-related diseases.Mitochondria are required for pro-ageing features of the senescent phenotype.The role of TGF-β1-miR-21-ROS pathway in bystander responses induced by irradiated non-small-cell lung cancer cells.The essence of senescence.The aging signature: a hallmark of induced pluripotent stem cells?The cytoprotective effect of N-acetyl-L-cysteine against ROS-induced cytotoxicity is independent of its ability to enhance glutathione synthesis.Combining ATR suppression with oncogenic Ras synergistically increases genomic instability, causing synthetic lethality or tumorigenesis in a dosage-dependent manner.MutT Homolog 1 (MTH1) maintains multiple KRAS-driven pro-malignant pathways.Investigation of cyanine dyes for in vivo optical imaging of altered mitochondrial membrane potential in tumors.Antagonistic TSC22D1 variants control BRAF(E600)-induced senescence.Mitochondrial effectors of cellular senescence: beyond the free radical theory of aging Reactive oxygen species production and mitochondrial dysfunction in white blood cells are not valid biomarkers of ageing in the very old Mitochondrial oxidative stress caused by Sod2 deficiency promotes cellular senescence and aging phenotypes in the skin.Oncogene-induced senescence results in marked metabolic and bioenergetic alterations Human Mut T Homolog 1 (MTH1): a roadblock for the tumor-suppressive effects of oncogenic RAS-induced ROS.RRM2B suppresses activation of the oxidative stress pathway and is up-regulated by p53 during senescence.EglN2 associates with the NRF1-PGC1α complex and controls mitochondrial function in breast cancer Differential Proteomic Analysis of Human Placenta-Derived Mesenchymal Stem Cells Cultured on Normal Tissue Culture Surface and Hyaluronan-Coated Surface.Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype.Pleiotropic actions of estrogen: a mitochondrial matter.Matched and mismatched metabolic fuels in lymphocyte function.AMPK Is Essential to Balance Glycolysis and Mitochondrial Metabolism to Control T-ALL Cell Stress and Survival.MicroRNA-15b regulates mitochondrial ROS production and the senescence-associated secretory phenotype through sirtuin 4/SIRT4 Tumor suppressor activity of the ERK/MAPK pathway by promoting selective protein degradation Arginase-II induces vascular smooth muscle cell senescence and apoptosis through p66Shc and p53 independently of its l-arginine ureahydrolase activity: implications for atherosclerotic plaque vulnerability

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P2860

Mitochondrial dysfunction contributes to oncogene-induced senescence.

http://www.wikidata.org/entity/Q39837656

description

2009 nî lūn-bûn

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2009年の論文

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年學術文章

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2009年學術文章

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2009年學術文章

@zh-hant

name

Mitochondrial dysfunction contributes to oncogene-induced senescence.

@en

Mitochondrial dysfunction contributes to oncogene-induced senescence.

@nl

type

label

Mitochondrial dysfunction contributes to oncogene-induced senescence.

@en

Mitochondrial dysfunction contributes to oncogene-induced senescence.

@nl

prefLabel

Mitochondrial dysfunction contributes to oncogene-induced senescence.

@en

Mitochondrial dysfunction contributes to oncogene-induced senescence.

@nl

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Molecular and Cellular Biology

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Mitochondrial dysfunction contributes to oncogene-induced senescence

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Antoine Roux

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Olga Moiseeva

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Véronique Bourdeau

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P2860

Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling

p53 has a direct apoptogenic role at the mitochondria

Phosphorylation of pRB at Ser612 by Chk1/2 leads to a complex between pRB and E2F-1 after DNA damage

A model for p53-induced apoptosis

Regulation of cellular response to oncogenic and oxidative stress by Seladin-1

Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a

Complete structure of the 11-subunit bovine mitochondrial cytochrome bc1 complex

Superoxide activates mitochondrial uncoupling proteins

Mitochondria: dynamic organelles in disease, aging, and development

Glycolytic enzymes can modulate cellular life span

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10.1128/MCB.01868-08

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16

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Xavier Deschênes-Simard

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