| First Author | Aiba Y | Year | 2008 |
| Journal | Blood | Volume | 111 |
| Issue | 3 | Pages | 1497-503 |
| PubMed ID | 18025150 | Mgi Jnum | J:130759 |
| Mgi Id | MGI:3772297 | Doi | 10.1182/blood-2007-08-109769 |
| Citation | Aiba Y, et al. (2008) Regulation of B-cell development by BCAP and CD19 through their binding to phosphoinositide 3-kinase. Blood 111(3):1497-503 |
| abstractText | 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. |
