| First Author | Wilker PR | Year | 2008 |
| Journal | Nat Immunol | Volume | 9 |
| Issue | 6 | Pages | 603-12 |
| PubMed ID | 18438409 | Mgi Jnum | J:136292 |
| Mgi Id | MGI:3795835 | Doi | 10.1038/ni.1609 |
| Citation | Wilker PR, et al. (2008) Transcription factor Mef2c is required for B cell proliferation and survival after antigen receptor stimulation. Nat Immunol 9(6):603-12 |
| abstractText | Calcineurin is required for B cell receptor (BCR)-induced proliferation of mature B cells. Paradoxically, loss of NFAT transcription factors, themselves calcineurin targets, induces hyperactivity, which suggests that calcineurin targets other than NFAT are required for BCR-induced proliferation. Here we demonstrate a function for the calcineurin-regulated transcription factor Mef2c in B cells. BCR-induced calcium mobilization was intact after Mef2c deletion, but loss of Mef2c caused defects in B cell proliferation and survival after BCR stimulation in vitro and lower T cell-dependent antibody responses and germinal center formation in vivo. Mef2c activity was specific to BCR stimulation, as Toll-like receptor and CD40 signaling induced normal responses in Mef2c-deficient B cells. Mef2c-dependent targets included the genes encoding cyclin D2 and the prosurvival factor Bcl-x(L). Our results emphasize an unrecognized but critical function for Mef2c in BCR signaling. |
