Document Detail


HTLV-1 HBZ suppresses AP-1 activity by impairing both the DNA-binding ability and the stability of c-Jun protein.
MedLine Citation:
PMID:  15592508     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Disruption of transcriptional control of cellular genes by human T-cell leukemia virus type-1 (HTLV-1) is thought to be associated, at least in part, with the development of adult T-cell leukemia. It has been reported that activating protein-1 (AP-1) is dysregulated by HTLV-1 infection. HTLV-1-encoded Tax elevates AP-1 activity through the induction of AP-1 family member gene expression, including c-Jun, JunD, c-Fos, and Fra-1. However, the precise mechanism by which HTLV-1 regulates AP-1 activity remains to be addressed. Recently, a novel viral protein named HTLV-1 basic leucine-zipper factor, HBZ, has been shown to interact with c-Jun and repress c-Jun-mediated transcription by abrogating its DNA-binding activity. In the course of investigating HBZ function, we found that HBZ reduced the steady-state levels of c-Jun, and the levels were restored by treatment with a proteasome inhibitor. Together, this indicates that HBZ promotes c-Jun degradation through a proteasome-dependent pathway. Furthermore, HBZ deletion mutants revealed that both the N-terminal and leucine-zipper region of HBZ were required for the elimination of c-Jun. These results suggest dual effects of HBZ on the suppression of AP-1 activity by inhibiting c-Jun function, which may contribute to the dysregulation of cell proliferation.
Authors:
Jun Matsumoto; Takayuki Ohshima; Osamu Isono; Kunitada Shimotohno
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Oncogene     Volume:  24     ISSN:  0950-9232     ISO Abbreviation:  Oncogene     Publication Date:  2005 Feb 
Date Detail:
Created Date:  2005-02-03     Completed Date:  2005-03-02     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8711562     Medline TA:  Oncogene     Country:  England    
Other Details:
Languages:  eng     Pagination:  1001-10     Citation Subset:  IM    
Affiliation:
Laboratory of Human Tumor Viruses, Department of Viral Oncology, Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606-8507, Japan.
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MeSH Terms
Descriptor/Qualifier:
Basic-Leucine Zipper Transcription Factors
DNA / genetics,  metabolism*,  pharmacology*
Gene Expression Regulation
Genes, jun
Hela Cells
Human T-lymphotropic virus 1 / genetics*,  pathogenicity*
Humans
Leucine Zippers
Leukemia-Lymphoma, Adult T-Cell / genetics,  virology
Proto-Oncogene Proteins c-jun / biosynthesis*,  pharmacology
Transcription Factor AP-1
Transcription Factors / pharmacology*
Transcription, Genetic
Tumor Cells, Cultured
Viral Proteins / pharmacology*
Chemical
Reg. No./Substance:
0/Basic-Leucine Zipper Transcription Factors; 0/HBZ protein, human T-cell leukemia virus type I; 0/Proto-Oncogene Proteins c-jun; 0/Transcription Factor AP-1; 0/Transcription Factors; 0/Viral Proteins; 9007-49-2/DNA

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