| First Author | Wen R | Year | 2003 |
| Journal | J Biol Chem | Volume | 278 |
| Issue | 44 | Pages | 43654-62 |
| PubMed ID | 12928432 | Mgi Jnum | J:86373 |
| Mgi Id | MGI:2679743 | Doi | 10.1074/jbc.M307318200 |
| Citation | Wen R, et al. (2003) Phospholipase Cgamma2 provides survival signals via Bcl2 and A1 in different subpopulations of B cells. J Biol Chem 278(44):43654-62 |
| abstractText | PLCgamma2 plays a critical role in B cell receptor (BCR) signaling and its targeted deletion results in defective B cell development and function. Here, we show that PLCgamma2 deficiency specifically blocks B cell maturation at the transitional type 2 (T2) to follicular (FO) B cell transition and the PLCgamma2 pathway regulates survival of B cells. BCR-induced apoptosis is dramatically enhanced in all subsets of splenic PLCgamma2-deficient B cells, especially in T2 and FO B cell subpopulations. We also find that all splenic PLCgamma2-deficient B cell subpopulations express abnormally low levels of Bcl-2 protein. In addition, PLCgamma2 deficiency disrupts BCR-mediated induction of A1 expression. Enforced expression of Bcl-2 prevents BCR-induced apoptosis in all splenic PLCgamma2-deficient B cell subpopulations and partially restores the numbers of PLCgamma2-deficient FO B cells. In contrast to Bcl-2, enforced expression of A1 preferentially prevents BCR-induced apoptosis in PLCgamma2-deficient FO B cells and partially restores the numbers of these B cells. Therefore, the PLCgamma2 pathway provides a survival signal via regulation of Bcl-2 in all splenic B cell subpopulations and via additional induction of A1 in mature FO B cells. |
