| First Author | Hamanaka Y | Year | 2022 |
| Journal | Biochem Biophys Res Commun | Volume | 603 |
| Pages | 1-6 | PubMed ID | 35259639 |
| Mgi Jnum | J:326714 | Mgi Id | MGI:7264128 |
| Doi | 10.1016/j.bbrc.2022.03.018 | Citation | Hamanaka Y, et al. (2022) Impaired B cell terminal differentiation in B cell-specific knockout mice of cell death-defying factor anamorsin. Biochem Biophys Res Commun 603:1-6 |
| abstractText | Anamorsin (AM) is an anti-apoptotic molecule cloned by us as a molecule that confers resistance against apoptosis induced by growth factor deprivation. AM-deficient mice are embryonic lethal, which impedes detailed analyses of the roles of AM in various types of adult cells. To overcome the embryonic lethality, we generated AM conditional knockout (AM(flox/flox)) mice and cell type-specific genetic modification became possible using the Cre-loxP system. CD19-Cre/AM(flox/flox) mice with AM deleted specifically in CD19(+) B cells exhibited less B220(+) B cells in their spleen, peripheral blood, and lymph node compared with control CD19-Cre mice. Using flow cytometry to categorize bone marrow and spleen cells into B cell subsets, we observed significantly less follicular type I cells, which are the most mature follicular B cells, compared with control CD19-Cre mice. These data suggest that AM has an important role in the generation of mature B cells. |
