| First Author | Jou ST | Year | 2002 |
| Journal | Mol Cell Biol | Volume | 22 |
| Issue | 24 | Pages | 8580-91 |
| PubMed ID | 12446777 | Mgi Jnum | J:80614 |
| Mgi Id | MGI:2446410 | Doi | 10.1128/MCB.22.24.8580-8591.2002 |
| Citation | Jou ST, et al. (2002) Essential, Nonredundant Role for the Phosphoinositide 3-Kinase p110delta in Signaling by the B-Cell Receptor Complex. Mol Cell Biol 22(24):8580-91 |
| abstractText | Many receptor and nonreceptor tyrosine kinases activate phosphoinositide 3-kinases (PI3Ks). To assess the role of the delta isoform of the p110 catalytic subunit of PI3Ks, we derived enzyme-deficient mice. The mice are viable but have decreased numbers of mature B cells, a block in pro-B-cell differentiation, and a B1 B-cell deficiency. Both immunoglobulin M receptor-induced Ca(2+) flux and proliferation in response to B-cell mitogens are attenuated. Immunoglobulin levels are decreased substantially. The ability to respond to T-cell-independent antigens is markedly reduced, and the ability to respond to T-cell-dependent antigens is completely eliminated. Germinal center formation in the spleen in response to antigen stimulation is disrupted. These results define a nonredundant signaling pathway(s) utilizing the delta isoform of p110 PI3K for the development and function of B cells. |
