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Titolo:
BLOCKAGE OF RNA-POLYMERASE AS A POSSIBLE TRIGGER FOR UV LIGHT-INDUCEDAPOPTOSIS
Autore:
LJUNGMAN M; ZHANG FF;
Indirizzi:
UNIV MICHIGAN,MED CTR,DEPT RADIAT ONCOL,DIV CANC BIOL ANN ARBOR MI 48109
Titolo Testata:
Oncogene
fascicolo: 4, volume: 13, anno: 1996,
pagine: 823 - 831
SICI:
0950-9232(1996)13:4<823:BORAAP>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSCRIPTION-COUPLED REPAIR; XERODERMA PIGMENTOSUM-CELLS; DNA-DAMAGE; COCKAYNES-SYNDROME; NUCLEAR ACCUMULATION; TORSIONAL TENSION; EXCISION-REPAIR; STRAND BREAKS; ACTIVE GENES; GROUP-C;
Keywords:
PREFERENTIAL REPAIR; P53; XERODERMA PIGMENTOSUM; COCKAYNES SYNDROME; UV LIGHT; IONIZING RADIATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
48
Recensione:
Indirizzi per estratti:
Citazione:
M. Ljungman e F.F. Zhang, "BLOCKAGE OF RNA-POLYMERASE AS A POSSIBLE TRIGGER FOR UV LIGHT-INDUCEDAPOPTOSIS", Oncogene, 13(4), 1996, pp. 823-831

Abstract

To study the triggering mechanism(s) of the induction of apoptosis following exposure to u.v. light, we used a genetic approach involving cell strains derived from patients with inherited deficiencies in nucleotide excision repair, It was found that cells from patients with Cockayne's syndrome, which are deficient in the processing of u.v.-inducedpyrimidine dimers from the transcribed DNA strand, are induced to undergo apoptosis at much lower doses of u.v. light than cells with proficient strand-specific repair, The induction of apoptosis correlated tothe induction of p53 and to the inhibition of total RNA and poly(A) mRNA synthesis, We also show that active p53 proteins accumulate following u.v.-irradiation without any apparent requirement for DNA strand breaks or excision repair intermediates, We propose that the blockage of RNA polymerases at DNA lesions in the transcribed strand triggers the induction of a pathway leading to apoptosis, These findings may helpexplain a long standing enigma of why, despite the DNA repair deficiency, patients with Cockayne's syndrome do not experience an elevated risk for skin cancer since potentially pre-mutagenic cells are eliminated by an easily triggered apoptotic pathway.

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Documento generato il 30/11/20 alle ore 06:03:47