Interstitial chromatin alteration causes persistent p53 activation involved in the radiation-induced senescence-like growth arrest

Biochemical and Biophysical Research Communications

Volumn 340, Issue 1, 2006, Pages 145-150

  Suzuki, Masatoshi ^a,c   Suzuki, Keiji ^a   Kodama, Seiji ^b   Watanabe, Masami ^c  

^a NAGASAKI UNIVERSITY   (Japan)

^b Osaka Prefecture University   (Japan)

^c KYOTO UNIVERSITY   (Japan)

Author keywords

ATM; Focus formation; Histone H2AX; Ionizing radiation; Persistent p53 activation; Premature cellular senescence; Senescence like growth arrest; Telomere

Indexed keywords

ATM PROTEIN; HISTONE H2AX; PROTEIN P53; SERINE;

ARTICLE; CELL AGING; CELL GROWTH; CHROMATIN; CONTROLLED STUDY; FLUORESCENCE IN SITU HYBRIDIZATION; GROWTH INHIBITION; HUMAN; HUMAN CELL; NORMAL HUMAN; PRIORITY JOURNAL; PROTEIN FUNCTION; PROTEIN LOCALIZATION; PROTEIN PHOSPHORYLATION; SENESCENCE; SIGNAL TRANSDUCTION; X IRRADIATION;

CELL AGING; CELL CYCLE; CELLS, CULTURED; CHROMATIN; CHROMOSOME ABERRATIONS; DIPLOIDY; DOSE-RESPONSE RELATIONSHIP, RADIATION; FIBROBLASTS; HUMANS; RADIATION DOSAGE; TUMOR SUPPRESSOR PROTEIN P53;

ATAXIA TELANGIECTASIA;

EID: 29244435335     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2005.11.167     Document Type: Article

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