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Prepublished online as a Blood First Edition Paper on June 26, 2003; DOI 10.1182/blood-2003-01-0173. This Article Full Text (PDF) All Versions of this Article: 2003-01-0173v1 102/8/2948    most recent Alert me when this article is cited Alert me if a correction is posted 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 Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Sanui, T. Articles by Fukui, Y. Search for Related Content PubMed PubMed Citation Articles by Sanui, T. Articles by Fukui, Y. Social Bookmarking                   What's this? Submitted January 23, 2003 Accepted June 19, 2003 DOCK2 regulates Rac activation and cytoskeletal reorganization through the interaction with ELMO1 Terukazu Sanui, Ayumi Inayoshi, Mayuko Noda, Eiko Iwata, Jens V Stein, Takehiko Sasazuki, and Yoshinori Fukui* Division of Immunogenetics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu Uiversity, Fukuoka, Japan Department of Immunology and Oncology, National Center for Biotechnology, Madrid, Spain The International Medical Center of Japan, Tokyo, Japan * Corresponding author; email: fukui{at}bioreg.kyushu-u.ac.jp. Although the migratory property of lymphocytes is critical for protective immunity, tissue infiltration of lymphocytes sometimes causes harmful immune responses. DOCK2 plays a critical role in lymphocyte migration by regulating actin cytoskeleton through Rac activation, yet the mechanism by which DOCK2 activates Rac remains unknown. We found that DOCK2 associates with ELMO1 through its SH3 domain. When DOCK2 was expressed in T hybridoma cells lacking endogenous expression of DOCK2, Rac activation and actin polymerization were induced. However, such responses were not elicited by the DOCK2 mutant lacking the region required for ELMO1-binding. On the other hand, we found that the expression of ELMO1 induces Rac activation in the plasmacytoma cells expressing DOCK2 but not ELMO1. These results indicate that the association of DOCK2 with ELMO1 is critical for DOCK2-mediated Rac activation, thereby suggesting that their association might be a therapeutic target for immunological disorders caused by lymphocyte infiltration. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Rauch, K. Pulkkinen, K. Saksela, and O. T. 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