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Blood, 1 February 2008, Vol. 111, No. 3, pp. 1497-1503. Prepublished online as a Blood First Edition Paper on November 19, 2007; DOI 10.1182/blood-2007-08-109769. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2007-08-109769v1 111/3/1497    most recent Alert me when this article is cited 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 Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Aiba, Y. Articles by Kurosaki, T. Search for Related Content PubMed PubMed Citation Articles by Aiba, Y. Articles by Kurosaki, T. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Regulation of B-cell development by BCAP and CD19 through their binding to phosphoinositide 3-kinase Yuichi Aiba1, Megumi Kameyama1, Tetsuo Yamazaki2, Thomas F. Tedder3, and Tomohiro Kurosaki1,2 1 Laboratory for Lymphocyte Differentiation, RIKEN Research Center for Allergy and Immunology, Tsurumi-ku, Yokohama, Japan; 2 Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, Moriguchi, Japan; 3 Department of Immunology, Duke University Medical Center, Durham, NC Despite the importance of phosphoinositide 3-kinase (PI3K) in B-cell development, its activation mechanism still remains elusive. In this study, we show that deletion of both BCAP and CD19 leads to an almost complete block of BCR-mediated Akt activation and to severe defects in generation of immature and mature B cells. The YXXM motifs in BCAP and CD19 are crucial for regulating B-cell development in that mutation of these motifs abrogated their ability to induce BCR-mediated Akt activation as well as to promote B-cell development. Furthermore, the developmental defect in CD19–/–BCAP–/– B cells was partly relieved by introducing a constitutively active form of PI3K or PDK1. Together, our data suggest that BCAP and CD19 have complementary roles in BCR-mediated PI3K activation, thereby, at least in part, contributing to B-cell development. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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