Linked Life Data

17786054

Source:http://linkedlifedata.com/resource/pubmed/id/17786054

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
20
pubmed:dateCreated
2007-10-24
pubmed:abstractText
Defective responses to DNA double strand breaks (DSBs) in the nervous system can lead to neurodegeneration or tumorigenesis. A key player in the repair of DNA DSBs is the tumor suppressor BRCA2, an essential component of the homologous recombination repair pathway and the Fanconi Anemia complex. We recently demonstrated that BRCA2 was required for normal neurogenesis and prevention of medulloblastoma brain tumors. Here, we discuss how this study contributes both to our understanding of BRCA2 functions in vivo, and the tissue-specific requirements for DNA repair and damage-signaling pathways.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1551-4005
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2453-7
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
BRCA2 function and the central nervous system.
pubmed:affiliation
Department of Genetics and Tumor Cell Biology, St Jude Children's Research Hospital, Memphis, Tennessee, USA.
pubmed:publicationType
Journal Article