HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

J. Biol. Chem., Vol. 275, Issue 27, 20382-20390, July 7, 2000

This Article Full Text Full Text (PDF) All Versions of this Article: 275/27/20382    most recent M001149200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Chen, P. Articles by Rapp, U. R. Search for Related Content PubMed PubMed Citation Articles by Chen, P. Articles by Rapp, U. R. Social Bookmarking                      What's this?

Transactivation of Naturally Occurring HIV-1 Long Terminal Repeats by the JNK Signaling Pathway
THE MOST FREQUENT NATURALLY OCCURRING LENGTH POLYMORPHISM SEQUENCE INTRODUCES A NOVEL BINDING SITE FOR AP-1 FACTORS^*

Peifeng Chen^§, Egbert Flory^§¶, Andris Avots, Bruce W. M. Jordan, Frank Kirchhoff^**, Stephan Ludwig, and Ulf R. Rapp

From the  Institut für Medizinische Strahlenkunde und Zellforschung, Universität Würzburg, Versbacher Strasse 5, D-97078 Würzburg, Germany, the ^** Institut für Klinische und Molekulare Virologie, Universität Erlangen, Schlogarten 4, D-91054 Erlangen, Germany, and the  Institut für Pathologie, Universität Würzburg, Joseph-Schneider-Strasse 2, D-97078 Würzburg, Germany

To study the role of MAPK cascades in the regulation of naturally occurring human immunodeficiency virus type 1 long terminal repeats (HIV-1 LTRs), we analyzed several HIV-1 LTRs from patients at different stages of disease progression. One of these naturally occurring HIV-1 LTRs contains an insertion termed the most frequent naturally occurring length polymorphism (MFNLP) and exhibited high inducibility upon T cell activation. We found that the protein kinase mixed lineage kinase 3/src-homology 3 domain-containing proline-rich kinase, a specific activator of the stress-activated protein kinase (SAPK)/JNK signaling pathway in T lymphocytes, induces high transcriptional activation of this promoter. Promoter inducibility is inhibited by the SAPK/JNK inhibitor, the JNK binding domain of the JNK interacting protein 1, and Tam-67 (N-terminal deletion mutant of c-Jun). In electrophoretic mobility shift assay, several protein complexes were found to bind to the MFNLP sequence in T cells. We identified AP-1 factors c-Fos and JunB as MFNLP-binding proteins, whose binding is abolished by introducing point mutations in the 3'-half of the MFNLP sequence. Introduction of these point mutations into the MFNLP containing HIV-1 LTR reduced src-homology 3 domain-containing proline-rich kinase -mediated transactivation. These data indicate that the AP-1-like binding site in the MFNLP sequence gives rise to a higher inducibility of natural HIV-LTRs by the SAPK/JNK signaling pathway.

CiteULike

Complore

Connotea

Del.icio.us

Digg

Reddit

Technorati

This article has been cited by other articles:

				C. Rizzi, M. P. Crippa, R. E. Jeeninga, B. Berkhout, F. Blasi, G. Poli, and M. Alfano Pertussis Toxin B-Oligomer Suppresses IL-6 Induced HIV-1 and Chemokine Expression in Chronically Infected U1 Cells via Inhibition of Activator Protein 1 J. Immunol., January 15, 2006; 176(2): 999 - 1006. [Abstract] [Full Text] [PDF]

				N. E. Faulkner, B. R. Lane, P. J. Bock, and D. M. Markovitz Protein Phosphatase 2A Enhances Activation of Human Immunodeficiency Virus Type 1 by Phorbol Myristate Acetate J. Virol., February 1, 2003; 77(3): 2276 - 2281. [Abstract] [Full Text] [PDF]

				R. K. Barr, T. S. Kendrick, and M. A. Bogoyevitch Identification of the Critical Features of a Small Peptide Inhibitor of JNK Activity J. Biol. Chem., March 22, 2002; 277(13): 10987 - 10997. [Abstract] [Full Text] [PDF]