Stress-induced premature senescence in hTERT-expressing ataxia telangiectasia fibroblasts. (Q52827047)

8 May 2018

title

Stress-induced premature senescence in hTERT-expressing ataxia telangiectasia fibroblasts. (English)

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8 May 2018

main subject

cell line

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ataxia telangiectasia

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Kazuhito Naka

1

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8 May 2018

Akira Tachibana

series ordinal

2

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8 May 2018

Kyoji Ikeda

series ordinal

3

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8 May 2018

Noboru Motoyama

series ordinal

4

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8 May 2018

language of work or name

English

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publication date

21 October 2003

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8 May 2018

Journal of Biological Chemistry

published in

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8 May 2018

volume

279

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8 May 2018

issue

3

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8 May 2018

page(s)

2030-2037

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8 May 2018

describes a project that uses

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Putting the stress on senescence

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The serial cultivation of human diploid cell strains

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Extension of life-span by introduction of telomerase into normal human cells

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Both Rb/p16INK4a inactivation and telomerase activity are required to immortalize human epithelial cells.

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

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Senescence of human fibroblasts induced by oncogenic Raf.

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Cellular and molecular mechanisms of stress-induced premature senescence (SIPS) of human diploid fibroblasts and melanocytes

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Induction of replicative senescence biomarkers by sublethal oxidative stresses in normal human fibroblast

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Oxidative stress shortens telomeres

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Expression of human telomerase (hTERT) does not prevent stress-induced senescence in normal human fibroblasts but protects the cells from stress-induced apoptosis and necrosis

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Sequential activation of the MEK-extracellular signal-regulated kinase and MKK3/6-p38 mitogen-activated protein kinase pathways mediates oncogenic ras-induced premature senescence

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Mitogen-activated protein kinase p38 defines the common senescence-signalling pathway

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The genetic defect in ataxia-telangiectasia

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Chromosome end associations, telomeres and telomerase activity in ataxia telangiectasia cells

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Accelerated telomere shortening in ataxia telangiectasia

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Ataxia telangiectasia mutant protein activates c-Abl tyrosine kinase in response to ionizing radiation

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Post-translational modifications and activation of p53 by genotoxic stresses

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DNA damage-induced activation of p53 by the checkpoint kinase Chk2

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Chk2 is a tumor suppressor that regulates apoptosis in both an ataxia telangiectasia mutated (ATM)-dependent and an ATM-independent manner

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Chk2-deficient mice exhibit radioresistance and defective p53-mediated transcription

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Characterization of ataxia telangiectasia fibroblasts with extended life-span through telomerase expression.

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Establishment of immortal normal and ataxia telangiectasia fibroblast cell lines by introduction of the hTERT gene

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Rescue of a telomere length defect of Nijmegen breakage syndrome cells requires NBS and telomerase catalytic subunit

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Telomerase and ATM/Tel1p protect telomeres from nonhomologous end joining

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Induction of ATF3 by ionizing radiation is mediated via a signaling pathway that includes ATM, Nibrin1, stress-induced MAPkinases and ATF-2.

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ATM deficiency and oxidative stress: a new dimension of defective response to DNA damage

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Mutations of the ATM gene detected in Japanese ataxia-telangiectasia patients: possible preponderance of the two founder mutations 4612del165 and 7883del5.

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A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia

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The Ataxia telangiectasia gene product is required for oxidative stress-induced G1 and G2 checkpoint function in human fibroblasts

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Uncoupling the senescent phenotype from telomere shortening in hydrogen peroxide-treated fibroblasts

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Pro-inflammatory cytokines and environmental stress cause p38 mitogen-activated protein kinase activation by dual phosphorylation on tyrosine and threonine

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Opposing effects of Ets and Id proteins on p16INK4a expression during cellular senescence

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DNA damage foci at dysfunctional telomeres

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Identifiers

DOI

10.1074/JBC.M309457200

1 reference

8 May 2018

PubMed ID

14570874

1 reference

8 May 2018