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

J. Biol. Chem., Vol. 282, Issue 3, 1830-1837, January 19, 2007

This Article Full Text Full Text (PDF) Supplemental Data All Versions of this Article: 282/3/1830    most recent M605666200v1 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 Mandicourt, G. Articles by Imhof, B. A. Search for Related Content PubMed PubMed Citation Articles by Mandicourt, G. Articles by Imhof, B. A. Social Bookmarking                      What's this?

JAM-C Regulates Tight Junctions and Integrin-mediated Cell Adhesion and Migration^*

Guillaume Mandicourt, Sandra Iden, Klaus Ebnet, Michel Aurrand-Lions, and Beat A. Imhof¹

From the Department of Pathology and Immunology, the University Medical Center, CH 1211 Geneva 4, Switzerland and the Institute of Medical Biochemistry, Center for Molecular Biology of Inflammation, University of Munster, D-48149 Münster, Germany

Junctional Adhesion Molecules (JAMs) have been described as major components of tight junctions in endothelial and epithelial cells. Tight junctions are crucial for the establishment and maintenance of cell polarity. During tumor development, they are remodeled, enabling neoplastic cells to escape from constraints imposed by intercellular junctions and to adopt a migratory behavior. Using a carcinoma cell line we tested whether JAM-C could affect tight junctions and migratory properties of tumor cells. We show that transfection of JAM-C improves the tight junctional barrier in tumor cells devoid of JAM-C expression. This is dependent on serine 281 in the cytoplasmic tail of JAM-C because serine mutation into alanine abolishes the specific localization of JAM-C in tight junctions and establishment of cell polarity. More importantly, the same mutation stimulates integrin-mediated cell migration and adhesion via the modulation of 1 and 3 integrin activation. These results highlight an unexpected function for JAM-C in controlling epithelial cell conversion from a static, polarized state to a pro-migratory phenotype.

Received for publication, June 13, 2006 , and in revised form, September 29, 2006.

^* This work was supported by Le Fonds National Suisse Grants 3100AO-100697/1 (to B. A. I.) and 310000-112551/1 (to M. A. L.), La Ligue Contre Le Cancer Grant OCS-01653-02-2005, and Deutsche Forschungsgemeinschaft Grant EB16012-3, SPP1111^* (to K. E.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Figs. S1-S4.

¹ To whom correspondence should be addressed: Dept. of Pathology and Immunology, University Medical Center, 1 Rue Michel-Servet, CH 1211 Geneva 4, Switzerland. Tel.: 41-22-379-57-47; Fax: 41-22-379-57-46; E-mail: beat.imhof{at}medecine.unige.ch.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				X. Li, M. Stankovic, B. P.-L. Lee, M. Aurrand-Lions, C. N. Hahn, Y. Lu, B. A. Imhof, M. A. Vadas, and J. R. Gamble JAM-C Induces Endothelial Cell Permeability Through Its Association and Regulation of {beta}3 Integrins Arterioscler. Thromb. Vasc. Biol., August 1, 2009; 29(8): 1200 - 1206. [Abstract] [Full Text] [PDF]

				M. Economopoulou, J. Hammer, F. Wang, R. Fariss, A. Maminishkis, and S. S. Miller Expression, Localization, and Function of Junctional Adhesion Molecule-C (JAM-C) in Human Retinal Pigment Epithelium Invest. Ophthalmol. Vis. Sci., March 1, 2009; 50(3): 1454 - 1463. [Abstract] [Full Text] [PDF]

				A. Praetor, J. M. McBride, H. Chiu, L. Rangell, L. Cabote, W. P. Lee, J. Cupp, D. M. Danilenko, and S. Fong Genetic deletion of JAM-C reveals a role in myeloid progenitor generation Blood, February 26, 2009; 113(9): 1919 - 1928. [Abstract] [Full Text] [PDF]

				A.-C. Luissint, P. G. Lutz, D. A. Calderwood, P.-O. Couraud, and S. Bourdoulous JAM-L-mediated leukocyte adhesion to endothelial cells is regulated in cis by {alpha}4{beta}1 integrin activation J. Cell Biol., December 15, 2008; 183(6): 1159 - 1173. [Abstract] [Full Text] [PDF]

				L. T. Braiterman, S. Heffernan, L. Nyasae, D. Johns, A. P. See, R. Yutzy, A. McNickle, M. Herman, A. Sharma, U. P. Naik, et al. JAM-A is both essential and inhibitory to development of hepatic polarity in WIF-B cells Am J Physiol Gastrointest Liver Physiol, February 1, 2008; 294(2): G576 - G588. [Abstract] [Full Text] [PDF]

				P. F. Bradfield, S. Nourshargh, M. Aurrand-Lions, and B. A. Imhof JAM Family and Related Proteins in Leukocyte Migration (Vestweber Series) Arterioscler. Thromb. Vasc. Biol., October 1, 2007; 27(10): 2104 - 2112. [Abstract] [Full Text] [PDF]

				P. F. Bradfield, C. Scheiermann, S. Nourshargh, C. Ody, F. W. Luscinskas, G. E. Rainger, G. B. Nash, M. Miljkovic-Licina, M. Aurrand-Lions, and B. A. Imhof JAM-C regulates unidirectional monocyte transendothelial migration in inflammation Blood, October 1, 2007; 110(7): 2545 - 2555. [Abstract] [Full Text] [PDF]

				C. Q.F. Wang and C. Y. Cheng A seamless trespass: germ cell migration across the seminiferous epithelium during spermatogenesis J. Cell Biol., August 9, 2007; 178(4): 549 - 556. [Abstract] [Full Text] [PDF]