| First Author | Clayton E | Year | 2002 |
| Journal | J Exp Med | Volume | 196 |
| Issue | 6 | Pages | 753-63 |
| PubMed ID | 12235209 | Mgi Jnum | J:79133 |
| Mgi Id | MGI:2387266 | Doi | 10.1084/jem.20020805 |
| Citation | Clayton E, et al. (2002) A crucial role for the p110delta subunit of phosphatidylinositol 3-kinase in B cell development and activation. J Exp Med 196(6):753-63 |
| abstractText | Mice lacking the p110delta catalytic subunit of phosphatidylinositol 3-kinase have reduced numbers of B1 and marginal zone B cells, reduced levels of serum immunoglobulins, respond poorly to immunization with type II thymus-independent antigen, and are defective in their primary and secondary responses to thymus-dependent antigen. p110delta(-/-) B cells proliferate poorly in response to B cell receptor (BCR) or CD40 signals in vitro, fail to activate protein kinase B, and are prone to apoptosis. p110delta function is required for BCR-mediated calcium flux, activation of phosphlipaseCgamma2, and Bruton's tyrosine kinase. Thus, p110delta plays a critical role in B cell homeostasis and function. |
