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Titolo:
Altered control of cellular proliferation in the absence of mammalian brahma (SNF2 alpha)
Autore:
Reyes, JC; Barra, J; Muchardt, C; Camus, A; Babinet, C; Yaniv, M;
Indirizzi:
Instceasteur, Unite Virus Oncogenes, CNRS, URA 1644, F-75724 Paris 15, Fran Inst Pasteur Paris France 15 nes, CNRS, URA 1644, F-75724 Paris 15, Fran Inst Pasteur, Unite Biol Dev, CNRS, URA 1960, F-75724 Paris, France Inst Pasteur Paris France F-75724 CNRS, URA 1960, F-75724 Paris, France
Titolo Testata:
EMBO JOURNAL
fascicolo: 23, volume: 17, anno: 1998,
pagine: 6979 - 6991
SICI:
0261-4189(199812)17:23<6979:ACOCPI>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
SWI-SNF COMPLEX; S-PHASE ENTRY; MICE LACKING; SACCHAROMYCES-CEREVISIAE; GLUCOCORTICOID RECEPTOR; RETINOBLASTOMA PROTEIN; TRANSCRIPTIONAL ACTIVATORS; CHROMATIN STRUCTURE; DROSOPHILA-BRAHMA; NUCLEOSOMAL DNA;
Keywords:
cell cycle; G(1) arrest; homologous recombination; SWI-SNF;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
64
Recensione:
Indirizzi per estratti:
Indirizzo: Yaniv, M Inst4Pasteur, Unite Virus Oncogenes, CNRS, URA 1644, 25 Rue Dr Roux, F-7572 Inst Pasteur 25 Rue Dr Roux Paris France 15 Rue Dr Roux, F-7572
Citazione:
J.C. Reyes et al., "Altered control of cellular proliferation in the absence of mammalian brahma (SNF2 alpha)", EMBO J, 17(23), 1998, pp. 6979-6991

Abstract

The mammalian SWI-SNF complex is an evolutionarily conserved, multi-subunit machine, involved in chromatin remodelling during transcriptional activation. Within this complex, the BRM (SNF2 alpha) and BRG1 (SNF2 beta) proteins are mutually exclusive subunits that are believed to affect nucleosomal structures using the energy of ATP hydrolysis. In order to characterize possible differences in the function of BRM and BRG1, and to gain further insights into the role of BRM-containing SWI-SNF complexes, the mouse BRM gene was inactivated by homologous recombination. BRM-/- mice develop normally, suggesting that an observed up-regulation of the BRG1 protein can functionally replace BRM in the SWI-SNF complexes of mutant cells. Nonetheless, adultmutant mice were similar to 15% heavier than control littermates. This maybe caused by increased cell proliferation, as demonstrated by a higher mitotic index detected in mutant livers. This is supported further by the observation that mutant embryonic fibroblasts were significantly deficient in their ability to arrest in the G(0)/G(1) phase of the cell cycle in responseto cell confluency or DNA damage. These studies suggest that BRM participates in the regulation of cell proliferation in adult mice.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/21 alle ore 03:09:49