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Titolo:
DNA double-strand breaks trigger apoptosis in p53-deficient fibroblasts
Autore:
Lips, J; Kaina, B;
Indirizzi:
Univ Mainz, Inst Toxicol, Div Appl Toxicol, D-55131 Mainz, Germany Univ Mainz Mainz Germany D-55131 iv Appl Toxicol, D-55131 Mainz, Germany
Titolo Testata:
CARCINOGENESIS
fascicolo: 4, volume: 22, anno: 2001,
pagine: 579 - 585
SICI:
0143-3334(200104)22:4<579:DDBTAI>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
WILD-TYPE P53; TUMOR-CELL LINES; CHROMOSOMAL-ABERRATIONS; RESTRICTION ENDONUCLEASES; HOMOLOGOUS RECOMBINATION; GEL-ELECTROPHORESIS; IONIZING-RADIATION; INDIVIDUAL CELLS; MAMMALIAN-CELLS; CHO CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Kaina, B Univ Mainz, Inst Toxicol, Div Appl Toxicol, Obere Zahlbacher Str 67, D-55131 Mainz, Germany Univ Mainz Obere Zahlbacher Str 67 Mainz Germany D-55131 Germany
Citazione:
J. Lips e B. Kaina, "DNA double-strand breaks trigger apoptosis in p53-deficient fibroblasts", CARCINOGENE, 22(4), 2001, pp. 579-585

Abstract

DNA double-strand breaks (DSBs) are induced by ionizing radiation (IR) andvarious radiomimetic agents directly, or indirectly as a consequence of DNA repair, recombination and replication of damaged DNA, They are ultimatelyinvolved in the generation of chromosomal aberrations and were reported tocause genomic instability, gene amplification and reproductive cell death. To address the question of whether DSBs act as a trigger of apoptosis, we induced DSBs by means of restriction enzyme electroporation and compared the effect with IR in mouse fibroblasts that differ in p53 status [wild-type (+/+) versus p53-deficient (-/-) cells]. We show that (i) electroporation of PvuII is highly efficient in the induction of DSBs, (ii) electroporation of PvuII increases the rate of apoptosis, but not of necrosis in p53-/- cells, (iii) treatment with gamma -rays induces both apoptosis and necrosis inp53-/- cells, (iv) the frequency of DSBs correlates with the yield of apoptosis and (v) both PvuII and gamma -ray treatment reduce the level of anti-apoptotic Bcl-2 protein in p53-/- cells whereas the level of Bar remains unaltered. Cells expressing wild-type p53 were more resistant than p53-deficient cells as to the induction of apoptosis and did not show Bcl-2 decline upon treatment with PvuII and gamma -rays, The data provide evidence that blunt-ended DSBs induced by restriction enzyme PvuII act as a highly efficient trigger of apoptosis, but not of necrosis, This process is related to Bcl-2 decline and does not require p53.

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Documento generato il 13/08/20 alle ore 14:38:53