Regulation of B-cell development by BCAP and CD19 through their binding to phosphoinositide 3-kinase.

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Aiba, Y; Kameyama, M; Yamazaki, T; Tedder, TF; Kurosaki, T

Published Date

  • February 1, 2008

Published In

Volume / Issue

  • 111 / 3

Start / End Page

  • 1497 - 1503

PubMed ID

  • 18025150

International Standard Serial Number (ISSN)

  • 0006-4971

Digital Object Identifier (DOI)

  • 10.1182/blood-2007-08-109769


  • eng

Conference Location

  • United States