| First Author | Su YW | Year | 2011 |
| Journal | Proc Natl Acad Sci U S A | Volume | 108 |
| Issue | 4 | Pages | 1555-60 |
| PubMed ID | 21205887 | Mgi Jnum | J:168328 |
| Mgi Id | MGI:4888053 | Doi | 10.1073/pnas.1017729108 |
| Citation | Su YW, et al. (2011) 14-3-3{sigma} regulates B-cell homeostasis through stabilization of FOXO1. Proc Natl Acad Sci U S A 108(4):1555-60 |
| abstractText | 14-3-3sigma regulates cytokinesis and cell cycle arrest induced by DNA damage but its role in the immune system is unknown. Using gene-targeted 14-3-3sigma-deficient (i.e., KO) mice, we studied the role of 14-3-3sigma in B-cell functions. Total numbers of B cells were reduced by spontaneous apoptosis of peripheral B cells. Upon B-cell antigen receptor engagement in vitro, KO B cells did not proliferate properly or up-regulate CD86. In response to T cell-independent antigens, KO B cells showed poor secretion of antigen-specific IgM. This deficit led to increased lethality of KO mice after vesicular stomatitis virus infection. KO B cells showed elevated total FOXO transcriptional activity but also increased FOXO1 degradation. Coimmunoprecipitation revealed that endogenous 14-3-3sigma protein formed a complex with FOXO1 protein. Our results suggest that 14-3-3sigma maintains FOXO1 at a consistent level critical for normal B-cell antigen receptor signaling and B-cell survival. |
