Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2007-5-2
pubmed:abstractText
Human RAD51 and RAD54 are key players in homologous recombination, a process that requires homology recognition and strand invasion by a RAD51-single-stranded DNA (ssDNA) nucleoprotein filament and chromatin remodeling by RAD54. Here we use in vitro chromatin reconstitution systems to show that RAD51-ssDNA stimulates RAD54-dependent chromatin remodeling in a homology-dependent, polarity-independent manner. This stimulation was not seen with RAD54B or other remodelers. Chromatin remodeling by RAD54 enabled strand invasion by RAD51-ssDNA on nucleosomal templates, which was homology- and polarity-dependent. Three natural RAD54 mutants found in primary cancer cells showed specific defects in remodeling or in the RAD54-RAD51 interaction. We propose that RAD54 is recruited by RAD51-ssDNA filament to the chromatin of the intact chromosome and that it remodels that chromatin to facilitate accessibility for strand exchange.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1545-9993
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
397-405
pubmed:dateRevised
2007-12-3
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Homology-driven chromatin remodeling by human RAD54.
pubmed:affiliation
Department of Molecular Biology, Massachusetts General Hospital and Department of Genetics, Harvard Medical School, 185 Cambridge Street, Boston, Massachusetts 02114, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural