JBC

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


     

Originally published In Press as doi:10.1074/jbc.M005067200 on January 29, 2001

J. Biol. Chem., Vol. 276, Issue 18, 14553-14561, May 4, 2001
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
276/18/14553    most recent
M005067200v1
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 Roy, J.
Right arrow Articles by Tremblay, M. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Roy, J.
Right arrow Articles by Tremblay, M. J.

Intercellular Adhesion Molecule-1 (ICAM-1) Gene Expression in Human T Cells Is Regulated by Phosphotyrosyl Phosphatase Activity
INVOLVEMENT OF NF-kappa B, Ets, AND PALINDROMIC INTERFERON-gamma -RESPONSIVE ELEMENT-BINDING SITES*

Jocelyn RoyDagger , Marie Audette§, and Michel J. Tremblay||

From the Centre de Recherche en Infectiologie, § Centre de Recherche en Oncologie et Endocrinologie Moléculaire, Centre Hospitalier Universitaire de Québec, Pavillon CHUL and Département de Biologie Médicale, Faculté de Médecine, Université Laval, Ste-Foy, Québec G1V 4G2, Canada

Intercellular adhesion molecule-1 (ICAM-1) plays an important role in adhesion phenomena involved in the immune response. The strength of adhesion has been shown to be modulated by changes in ICAM-1 gene expression. In T cells, signaling pathways are intimately regulated by an equilibrium between protein-tyrosine kinases and protein tyrosine phosphatases (PTP). The use of bis-peroxovanadium (bpV) compounds, a class of potent PTP inhibitors, enabled us to investigate the involvement of phosphotyrosyl phosphatases in the regulation of ICAM-1 gene expression in human T cells. Here, we demonstrate for the first time that inhibition of PTP results in an increase of ICAM-1 surface expression on both human T lymphoid and primary mononuclear cells. The crucial role played by the NF-kappa B-, Ets-, and pIgamma RE-binding sites in bpV[pic]-mediated activation of ICAM-1 was demonstrated using various 5' deletion and site-specific mutants of the ICAM-1 gene promoter driving the luciferase reporter gene. Co-transfection experiments with trans-dominant mutants and electrophoretic mobility shift assays confirmed the importance of constitutive and inducible transcription factors that bind to specific responsive elements in bpV-dependent up-regulation of ICAM-1 surface expression. Altogether, these observations suggest that expression of ICAM-1 in human T cells is regulated by phosphotyrosyl phosphatase activity through NF-kappa B-, Ets-, and STAT-1-dependent signaling pathways.

* This work was supported in part by Grant HOP-15575 from the Canadian Institutes of Health Research HIV/AIDS Research Program (to M. J. T.).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.

Dagger Submitted in partial fulfillment for the M.Sc. degree from the Microbiology-Immunology Program, Faculty of Medicine, Laval University.

Recipient of a Chercheur National award from the Fonds de la Recherche en Santé du Québec.

|| Holds a Canada Research Chair in Human Immuno-Retrovirology and recipient of Canadian Institutes of Health Research Investigator award. To whom correspondence should be addressed: Laboratoire d'Immuno-Rétrovirologie Humaine, Centre de Recherche en Infectiologie, RC709, Centre Hospitalier Universitaire de Québec, Pavillon CHUL, 2705 Blvd. Laurier, Ste-Foy, Québec G1V 4G2, Canada. Tel.: 418-654-2705; Fax: 418-654-2212; E-mail: Michel.J.Tremblay@crchul.ulaval.ca.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.


This article has been cited by other articles:


Home page
 J. Immunol.Home page
S. Thibault, M. R. Tardif, C. Barat, and M. J. Tremblay
TLR2 Signaling Renders Quiescent Naive and Memory CD4+ T Cells More Susceptible to Productive Infection with X4 and R5 HIV-Type 1
J. Immunol., October 1, 2007; 179(7): 4357 - 4366.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
M. I. Garcia, J. Kaserman, Y.-H. Chung, J. U. Jung, and S.-H. Lee
Herpesvirus Saimiri STP-A Oncoprotein Utilizes Src Family Protein Tyrosine Kinase and Tumor Necrosis Factor Receptor-Associated Factors To Elicit Cellular Signal Transduction
J. Virol., March 15, 2007; 81(6): 2663 - 2674.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
J.-F. Fortin, C. Barat, Y. Beausejour, B. Barbeau, and M. J. Tremblay
Hyper-responsiveness to Stimulation of Human Immunodeficiency Virus-infected CD4+ T Cells Requires Nef and Tat Virus Gene Products and Results from Higher NFAT, NF-{kappa}B, and AP-1 Induction
J. Biol. Chem., September 17, 2004; 279(38): 39520 - 39531.
[Abstract] [Full Text] [PDF]

Home page
 J. Pharmacol. Exp. Ther.Home page
X.-L. Chen, Q. Zhang, R. Zhao, X. Ding, P. E. Tummala, and R. M. Medford
Rac1 and Superoxide Are Required for the Expression of Cell Adhesion Molecules Induced by Tumor Necrosis Factor-alpha in Endothelial Cells
J. Pharmacol. Exp. Ther., May 1, 2003; 305(2): 573 - 580.
[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 © 2001 by the American Society for Biochemistry and Molecular Biology.