JBC PeproTech; Our Business is Cytokines!

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Originally published In Press as doi:10.1074/jbc.M211167200 on December 24, 2002

J. Biol. Chem., Vol. 278, Issue 14, 12310-12318, April 4, 2003
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
278/14/12310    most recent
M211167200v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Harrod, R.
Right arrow Articles by Franchini, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Harrod, R.
Right arrow Articles by Franchini, G.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Human Immunodeficiency Virus Type-1 Tat/Co-activator Acetyltransferase Interactions Inhibit p53Lys-320 Acetylation and p53-responsive Transcription*

Robert HarrodDagger §, Janos Nacsa, Carine Van Lint||**, Jeremy Hansen, Tatiana KarpovaDagger Dagger , James McNallyDagger Dagger , and Genoveffa Franchini

From the Dagger  Laboratory of Molecular Virology, Department of Biological Sciences, Southern Methodist University, Dallas, Texas 75275-0376, the  Basic Research Laboratory, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892-0001, the || Université Libre de Bruxelles, Institut de Biologie et de Medecine, Moleculaires, Service de Chimie Biologique, Laboratoire de Virologie, Moleculaire, 6041 Gosselies, Belgium, and the Dagger Dagger  Laboratory of Receptor Biology and Gene Expression, Fluorescence, Imaging Facility, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892-0001

Patients with AIDS are at increased risk for developing various neoplasms, including Hodgkin's and non-Hodgkin's lymphomas, Kaposi's sarcomas, and anal-rectal carcinomas, suggestive that human immunodeficiency virus type-1 infection might promote establishment of AIDS-related cancers. Tat, the viral trans-activator, can be endocytosed by uninfected cells and has been shown to inhibit p53 functions, providing a candidate mechanism through which the human immunodeficiency virus type-1 might contribute to malignant transformation. Because Tat has been shown to interact with histone acetyltransferase domains of p300/cAMP-responsive element-binding protein (CREB)-binding protein and p300/CREB-binding protein-associated factor, we have investigated whether Tat might alter p53 acetylation and tumor suppressor-responsive transcription. Here, we demonstrate that both Tat and p53 co-localize with p300/CREB-binding protein-associated factor and p300 in nuclei of IMR-32 human neuroblastoma cells and in PC-12 pheochromocytoma cells. Further, p53 trans-activation of the 14-3-3sigma promoter was markedly repressed by Tat-histone acetyltransferase interactions, and p53 acetylation by p300/CREB-binding protein-associated factor on residue Lys320 was diminished as a result of Tat-histone acetyltransferase binding in vivo and in vitro. Tat also inhibited p53 acetylation by p300 in a dosage-dependent manner in vitro. Finally, HIV-1-infected Molt-4 cells displayed reduced p53 acetylation on lysines 320 and 373 in response to UV irradiation. Our results allude to a mechanism whereby the human immunodeficiency virus type-1 trans-activator might impair tumor suppressor functions in immune/neuronal-derived cells, thus favoring the establishment of neoplasia during AIDS.

* This work was supported by the NCI, National Institutes of Health, and in part by the Department of Biological Sciences of Southern Methodist University.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ To whom correspondence should be addressed: Lab. of Molecular Virology, Dept. of Biological Sciences, Southern Methodist University, 334-DLS, 6501 Airline Dr., Dallas, TX 75275-0376. Tel.: 214-768-3864; Fax: 214-768-3955; E-mail: rharrod@mail.smu.edu.

** Maître de Recherches from the Fonds National de la Recherche Scientifique (Belgium). Supported by the Fonds National de la Recherche Scientifique, Televie, Free University of Brussels (ARC), Internationale Brachet Stiftung, CGRI-INSERM cooperation, the Theyskens-Mineur Foundation, Region Wallone-Commission Europeenne FEDER, and the Agence Nationale de Recherches sur le SIDA (ANRS, France).

Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
A. Sharma, S. Awasthi, C. K. Harrod, E. F. Matlock, S. Khan, L. Xu, S. Chan, H. Yang, C. K. Thammavaram, R. A. Rasor, et al.
The Werner Syndrome Helicase Is a Cofactor for HIV-1 Long Terminal Repeat Transactivation and Retroviral Replication
J. Biol. Chem., April 20, 2007; 282(16): 12048 - 12057.
[Abstract] [Full Text] [PDF]

Home page
 J. Leukoc. Biol.Home page
E. Pauls, J. Senserrich, B. Clotet, and J. A. Este
Inhibition of HIV-1 replication by RNA interference of p53 expression
J. Leukoc. Biol., September 1, 2006; 80(3): 659 - 667.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
S. Amini, G. Mameli, L. Del Valle, A. Skowronska, K. Reiss, B. B. Gelman, M. K. White, K. Khalili, and B. E. Sawaya
p73 Interacts with Human Immunodeficiency Virus Type 1 Tat in Astrocytic Cells and Prevents Its Acetylation on Lysine 28
Mol. Cell. Biol., September 15, 2005; 25(18): 8126 - 8138.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
K. Wong, A. Sharma, S. Awasthi, E. F. Matlock, L. Rogers, C. Van Lint, D. J. Skiest, D. K. Burns, and R. Harrod
HIV-1 Tat Interactions with p300 and PCAF Transcriptional Coactivators Inhibit Histone Acetylation and Neurotrophin Signaling through CREB
J. Biol. Chem., March 11, 2005; 280(10): 9390 - 9399.
[Abstract] [Full Text] [PDF]

Home page
 J. Leukoc. Biol.Home page
O. Rohr, C. Marban, D. Aunis, and E. Schaeffer
Regulation of HIV-1 gene transcription: from lymphocytes to microglial cells
J. Leukoc. Biol., November 1, 2003; 74(5): 736 - 749.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 All ASBMB Journals   Molecular and Cellular Proteomics 
 Journal of Lipid Research   ASBMB Today 
Copyright © 2003 by the American Society for Biochemistry and Molecular Biology.