Abstract:
: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.
journal_name
Bloodjournal_title
Bloodauthors
Aiba Y,Kameyama M,Yamazaki T,Tedder TF,Kurosaki Tdoi
10.1182/blood-2007-08-109769subject
Has Abstractpub_date
2008-02-01 00:00:00pages
1497-503issue
3eissn
0006-4971issn
1528-0020pii
blood-2007-08-109769journal_volume
111pub_type
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