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Titolo:
A MUTATION IN THE P53 TUMOR-SUPPRESSOR GENE OF AHH-1 TK(+ -) HUMAN LYMPHOBLASTOID-CELLS/
Autore:
MORRIS SM; MANJANATHA MG; SHELTON SD; DOMON OE; MCGARRITY LJ; CASCIANO DA;
Indirizzi:
US FDA,DIV GENET TOXICOL,NATL CTR TOXICOL RES,DEPT HLTH & HUMAN SERV,HFT 120,3900 NCTR RD JEFFERSON AR 72079
Titolo Testata:
Mutation research
fascicolo: 2, volume: 356, anno: 1996,
pagine: 129 - 134
SICI:
0027-5107(1996)356:2<129:AMITPT>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
WILD-TYPE P53; MUTANT P53; HUMAN CANCERS; APOPTOSIS; INDUCTION; PROTEIN; LINE; SENSITIVITY; COMPETENT; MUTAGEN;
Keywords:
AHH-1 TK(+/-) HUMAN LYMPHOBLASTOID CELL; MCL-5 HUMAN LYMPHOBLASTOID CELL; P53 MUTATION; CPG MUTATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
33
Recensione:
Indirizzi per estratti:
Citazione:
S.M. Morris et al., "A MUTATION IN THE P53 TUMOR-SUPPRESSOR GENE OF AHH-1 TK(+ -) HUMAN LYMPHOBLASTOID-CELLS/", Mutation research, 356(2), 1996, pp. 129-134

Abstract

Loss-of-function mutations in the p53 tumor suppressor gene result inan altered response to DNA-damaging agents. Included in the mutant p53 phenotype are the loss of the G(1) checkpoint and delayed apoptotic cell death, characteristics we have consistently observed in the the AHH-1 tk(+/-) cell line following exposure to DNA-damaging agents. In order to determine the functional status of p53 in the AHH-1 tk(+/-) cell line, molecular analysis (single-strand conformational polymorphism[SSCP] and sequence analysis) was performed on exons 5-9 of the p53 gene. In addition, the status of the p53 gene in the closely related lymphoblast line, MCL-5, which, in our hands, has a much higher spontaneous rate of apoptosis than AHH-1 tk(+/-), was also determined by molecular analysis. Initial SSCP analysis of AHH-1 tk(+/-) revealed an abnormal migration pattern of exon 8 when compared to a wild-type control. Subsequent sequence analysis indicated that a base-pair substitution ((C) under bar GG --> (T) under bar GG) mutation had occurred at codon282, a reported 'hot spot' for 5-methylcytosine mutations in the human p53 gene. Neither SSCP nor sequence analysis of exons 5-9 of MCL-5 indicated any differences from wild-type DNA. These results suggest that the lack of a G(1) arrest and the delayed entrance into apoptosis observed in chemically-exposed AHH-1 tk(+/-) cells are, at least partially, accounted for by a loss-of-function mutation in the p53 gene.

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Documento generato il 06/04/20 alle ore 07:59:20