DNA damaging agents and p53 do not cause senescence in quiescent cells, while consecutive re-activation of mTOR is associated with conversion to senescence - Wikidata - awgldk - TriplyDB

DNA damaging agents and p53 do not cause senescence in quiescent cells, while consecutive re-activation of mTOR is associated with conversion to senescence

DNA damaging agents and p53 do not cause senescence in quiescent cells, while consecutive re-activation of mTOR is associated with conversion to senescence

http://www.wikidata.org/entity/Q28972513

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Reprogramming of energy metabolism as a driver of aging Rapalogs in cancer prevention: anti-aging or anticancer?Radiation-Induced Bystander Response: Mechanism and Clinical Implications Advances in targeting signal transduction pathways Suppression of replicative senescence by rapamycin in rodent embryonic cells Big mice die young but large animals live longer Dysregulated ΔNp63α inhibits expression of Ink4a/arf, blocks senescence, and promotes malignant conversion of keratinocytes Elimination of proliferating cells unmasks the shift from senescence to quiescence caused by rapamycin Contact inhibition and high cell density deactivate the mammalian target of rapamycin pathway, thus suppressing the senescence program Hyper-mitogenic drive coexists with mitotic incompetence in senescent cells.DNA damage causes TP53-dependent coupling of self-renewal and senescence pathways in embryonal carcinoma cells Disruption of clathrin-mediated trafficking causes centrosome overduplication and senescence.From rapalogs to anti-aging formula.Hormesis, cell death and aging.A set of miRNAs participates in the cellular senescence program in human diploid fibroblasts.Interaction between the Cockayne syndrome B and p53 proteins: implications for aging Hypoxia suppresses conversion from proliferative arrest to cellular senescence.Selective anti-cancer agents as anti-aging drugs Sensitive detection and monitoring of senescence-associated secretory phenotype by SASP-RAP assay.Potential anti-aging agents suppress the level of constitutive mTOR- and DNA damage- signaling Senescence of tumor cells induced by oxaliplatin increases the efficiency of a lipid A immunotherapy via the recruitment of neutrophils.Inhibition of IGF-1R prevents ionizing radiation-induced primary endothelial cell senescence Inflammation and p53: A Tale of Two Stresses Tumor promoter-induced cellular senescence: cell cycle arrest followed by geroconversion.Involvement of Akt and mTOR in chemotherapeutic- and hormonal-based drug resistance and response to radiation in breast cancer cells.Cooperative effects of Akt-1 and Raf-1 on the induction of cellular senescence in doxorubicin or tamoxifen treated breast cancer cells.NUAK2: an emerging acral melanoma oncogene Hormesis does not make sense except in the light of TOR-driven aging.Molecular damage in cancer: an argument for mTOR-driven aging Recent progress in targeting cancer.NCI's provocative questions on cancer: some answers to ignite discussion.Chitosan Treatment Delays the Induction of Senescence in Human Foreskin Fibroblast Strains.Genome integrity, stem cells and hyaluronan.AKT induces senescence in human cells via mTORC1 and p53 in the absence of DNA damage: implications for targeting mTOR during malignancy.Cell cycle arrest is not yet senescence, which is not just cell cycle arrest: terminology for TOR-driven aging.Transcriptional regulation of gene expression during osmotic stress responses by the mammalian target of rapamycin.Geroconversion: irreversible step to cellular senescence Tumor suppression by p53 without apoptosis and senescence: conundrum or rapalog-like gerosuppression?Wt p53 impairs response to chemotherapy: make lemonade to spare normal cells Rejuvenating immunity: "anti-aging drug today" eight years later.

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P2860

DNA damaging agents and p53 do not cause senescence in quiescent cells, while consecutive re-activation of mTOR is associated with conversion to senescence

http://www.wikidata.org/entity/Q28972513

description

2010 nî lūn-bûn

@nan

2010 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի դեկտեմբերին հրատարակված գիտական հոդված

@hy

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

@zh-hk

2010年論文

@zh-mo

2010年論文

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2010年论文

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name

DNA damaging agents and p53 do ...... with conversion to senescence

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DNA damaging agents and p53 do ...... with conversion to senescence

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DNA damaging agents and p53 do ...... with conversion to senescence

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DNA damaging agents and p53 do ...... with conversion to senescence

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DNA damaging agents and p53 do ...... with conversion to senescence

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DNA damaging agents and p53 do ...... with conversion to senescence

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DNA damaging agents and p53 do ...... with conversion to senescence

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Blagosklonny MV

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Leontieva OV

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P2860

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

Phosphate-activated glutaminase (GLS2), a p53-inducible regulator of glutamine metabolism and reactive oxygen species

Glutaminase 2, a novel p53 target gene regulating energy metabolism and antioxidant function

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

Analysis of DRAM-related proteins reveals evolutionarily conserved and divergent roles in the control of autophagy

TOR signaling in growth and metabolism

TOR, a central controller of cell growth.

p53 target genes sestrin1 and sestrin2 connect genotoxic stress and mTOR signaling

Topoisomerase II-mediated DNA damage is differently repaired during the cell cycle by non-homologous end joining and homologous recombination

Pseudo-DNA damage response in senescent cells

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924-935

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scholarly article

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4855716

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10.18632/AGING.100265

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12

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2

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3034181

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