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Titolo:
The RadB protein from Pyrococcus does not complement E-coli recA mutationsin vivo
Autore:
Inwood, W; Kane, S; DiRuggiero, J; Robb, F; Clark, AJ;
Indirizzi:
Univ Calif Berkeley, Lawrence Berkeley Lab, Dept Mol & Cell Biol, Div LifeSci, Berkeley, CA 94720 USA Univ Calif Berkeley Berkeley CA USA 94720 LifeSci, Berkeley, CA 94720 USA Univ Maryland, Inst Biotechnol, Ctr Marine Biotechnol, Baltimore, MD 21201USA Univ Maryland Baltimore MD USA 21201 e Biotechnol, Baltimore, MD 21201USA Univ Arizona, Dept Mol & Cellular Biol, Tucson, AZ 85721 USA Univ ArizonaTucson AZ USA 85721 ol & Cellular Biol, Tucson, AZ 85721 USA
Titolo Testata:
MOLECULAR GENETICS AND GENOMICS
fascicolo: 4, volume: 265, anno: 2001,
pagine: 683 - 686
SICI:
1617-4615(200106)265:4<683:TRPFPD>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
DNA STRAND EXCHANGE; HYPERTHERMOPHILIC ARCHAEON; RECA/RAD51 HOMOLOG; ESCHERICHIA-COLI; SACCHAROMYCES-CEREVISIAE; GLUTAMATE-DEHYDROGENASE; FURIOSUS; EXPRESSION; POLYMERASE; BINDING;
Keywords:
radB gene; Pyrococcus furiosus; recA gene; recombination; repair of UV damage;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
24
Recensione:
Indirizzi per estratti:
Indirizzo: Clark, AJ Univ Calif Berkeley, Lawrence Berkeley Lab, Dept Mol & Cell Biol, Div LifeSci, Berkeley, CA 94720 USA Univ Calif Berkeley Berkeley CA USA 94720 erkeley, CA 94720 USA
Citazione:
W. Inwood et al., "The RadB protein from Pyrococcus does not complement E-coli recA mutationsin vivo", MOL GENET G, 265(4), 2001, pp. 683-686

Abstract

A previous publication claimed that the radB gene called Pk-REC from Pyrococcus furiosus complemented an E. coli recA mutation. We found that a sequencing error had led to the test of a mutant form of Pk-REC. The wild-type radB gene from P. furiosus cloned in a similar expression vector to the mutant Pk-REC also appeared to complement an E. coh recA mutation. However, thecloned P. furiosus gdh (glutamate dehydrogenase) gene showed the same activity. We therefore concluded that overexpression of any protein can producean artificial growth inhibition or stationary phase in recA mutant cells, which allows cells to recover from UV damage due to the action of repair systems that do not require RecA-like activity.

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Documento generato il 29/03/20 alle ore 08:56:40