Linked Life Data

9788437

Source:http://linkedlifedata.com/resource/pubmed/id/9788437

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
15
pubmed:dateCreated
1998-11-6
pubmed:abstractText
c-Myc, a proto-oncogene that is implicated in tumorigenesis, embryonic development and apoptosis, can physically associate with BRCA1. We have found that BRCA1 interacts with c-Myc in yeast, in in vitro assays and in mammalian cells. Endogenous interactions between BRCA1 and c-Myc were also observed. Efficient BRCA1-Myc association requires the intact helix-loop-helix region of c-Myc, a motif involved in Myc-Max dimerization. BRCA1 does not however bind to Max. Our studies revealed that BRCA1 represses Myc-mediated transcription while having no effect on some other transcriptional activities. Furthermore, BRCA1 reverses the phenotype of embryonic fibroblasts transformed by the activation of Myc and Ras, but only minimally affects the transformed phenotype induced by SV40 virus. These data indicate that BRCA1 may function as a tumor suppressor by regulating the behavior of c-Myc and provide a molecular explanation for some of the effects of the BRCA1 gene product.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1939-48
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
BRCA1 binds c-Myc and inhibits its transcriptional and transforming activity in cells.
pubmed:affiliation
Department of Pathology, University of Pennsylvania School of Medicine, Philadelphia 19104, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't