| First Author | Khiem D | Year | 2008 |
| Journal | Proc Natl Acad Sci U S A | Volume | 105 |
| Issue | 44 | Pages | 17067-72 |
| PubMed ID | 18955699 | Mgi Jnum | J:144071 |
| Mgi Id | MGI:3829850 | Doi | 10.1073/pnas.0804868105 |
| Citation | Khiem D, et al. (2008) A p38 MAPK-MEF2C pathway regulates B-cell proliferation. Proc Natl Acad Sci U S A 105(44):17067-72 |
| abstractText | B lymphocytes are an integral part of the adaptive immune system. On antigen binding to the B-cell receptor (BCR), B cells rapidly proliferate and differentiate into antibody-secreting plasma cells. The p38 mitogen-activated protein kinase (MAPK) pathway functions downstream of the BCR to control cell proliferation, but the transcriptional effectors of this pathway in B cells have remained elusive. In the present study, we inactivated Mef2c exclusively in B cells by conditional gene targeting in mice. Loss of MEF2C function resulted in a reduced immune response to antigen, defective germinal center formation, and a severe defect in B-cell proliferation, and we show that MEF2C regulates proliferation in response to BCR stimulation via the p38 MAPK pathway. p38 directly phosphorylates MEF2C via three residues in the C-terminal transactivation domain, establishing MEF2C as a direct transcriptional effector of BCR signaling via p38 MAPK. |
