| First Author | Xing Y | Year | 2005 |
| Journal | J Exp Med | Volume | 202 |
| Issue | 5 | Pages | 707-19 |
| PubMed ID | 16129705 | Mgi Jnum | J:100706 |
| Mgi Id | MGI:3589325 | Doi | 10.1084/jem.20050637 |
| Citation | Xing Y, et al. (2005) Protein phosphatase subunit G5PR is needed for inhibition of B cell receptor-induced apoptosis. J Exp Med 202(5):707-19 |
| abstractText | B cell receptor (BCR) cross-linking induces B cell proliferation and sustains survival through the phosphorylation-dependent signals. We report that a loss of the protein phosphatase component G5PR increased the activation-induced cell death (AICD) and thus impaired B cell survival. G5PR associates with GANP, whose expression is up-regulated in mature B cells of the peripheral lymphoid organs. To study G5PR function, the G5pr gene was conditionally targeted with the CD19-Cre combination (G5pr(-/-) mice). The G5pr(-/-) mice had a decreased number of splenic B cells (60% of the controls). G5pr(-/-) B cells showed a normal proliferative response to lipopolysaccharide or anti-CD40 antibody stimulation but not to BCR cross-linking with or without IL-4 in vitro. G5pr(-/-) B cells did not show abnormalities in the BCR-mediated activation of Erks and NF-kappaB, cyclin D2 induction, or Akt activation. However, G5pr(-/-) B cells were sensitive to AICD caused by BCR cross-linking. This was associated with an increased depolarization of the mitochondrial membrane and the enhanced activation of c-Jun NH(2)-terminal protein kinase and Bim. These results suggest that G5PR is required for the BCR-mediated proliferation associated with the prevention of AICD in mature B cells. |
