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PMID: 12080089 Published · ppublish English Journal Article Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S.

JunB potentiates function of BRCA1 activation domain 1 (AD1) through a coiled-coil-mediated interaction.

Genes & development ·Vol. 16 ·No. 12 ·2002-06-15 ·Pages 1509-17

Hu YF, Li R

Abstract

BRCA1 is involved in the regulation of multiple nuclear events including transcription. AD1, one of the two trans-activation domains in BRCA1, stimulates transcription in a cell context-dependent manner. Here, it is shown that BRCA1 interacts with Jun proteins via a coiled-coil motif in AD1 and the basic leucine zipper (bZIP) region of the Jun proteins. The Jun-interacting domain in BRCA1 is critical for AD1-mediated transcriptional activation. In particular, the strength of AD1 in transcriptional activation is limited by the JunB level and ectopic expression of JunB potentiates the transcriptional activity of AD1. Furthermore, JunB mRNA expression is down-regulated in many ovarian tumor tissues examined. Thus, the coiled-coil-mediated cooperation between BRCA1 and JunB may facilitate the function of these proteins in tissue-specific transcriptional regulation and tumor suppression.

MeSH Terms
BRCA1 Protein/chemistry Cell Line Genetic Vectors Glutathione Transferase/metabolism Humans Polymerase Chain Reaction Precipitin Tests Protein Binding Protein Structure, Tertiary Proto-Oncogene Proteins c-jun/metabolism Transcriptional Activation Two-Hybrid System Techniques
Chemicals
BRCA1 Protein Proto-Oncogene Proteins c-jun Glutathione Transferase
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Hu Yan-Fen
Department of Biochemistry and Molecular Genetics, School of Medicine, University of Virginia, Charlottesville 22908, USA.
Li Rong
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Article Info
Journal
Genes & development
Abbr.
Genes Dev
ISSN
0890-9369
DOI
10.1101/gad.995502
Published
2002-06-15
Pages
1509-17
Language
English
Region
United States
NLM ID
8711660
PMCID
PMC186344
Subset
IM
External Links
PubMed source DOI: 10.1101/gad.995502 PMC Full Text View journal details
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