| First Author | Yabe D | Year | 2007 |
| Journal | Genesis | Volume | 45 |
| Issue | 5 | Pages | 300-6 |
| PubMed ID | 17457934 | Mgi Jnum | J:121523 |
| Mgi Id | MGI:3710394 | Doi | 10.1002/dvg.20296 |
| Citation | Yabe D, et al. (2007) Generation of a conditional knockout allele for mammalian Spen protein Mint/SHARP. Genesis 45(5):300-6 |
| abstractText | The Spen protein family is found in worms, flies, and mammals, and is implicated in diverse biological processes from embryogenesis to aging. Spen proteins have three N-terminal RNA recognition motifs and a C-terminal SPOC domain. The mammalian Spen proteins Mint and its human ortholog SHARP interact with the Notch-signaling mediator RBP-J as well as Msx2 and several unliganded nuclear hormone receptors, and impart transcription-repressing activity to these molecules by recruiting corepressors through the SPOC domain. Despite these in vitro findings, Mint/SHARP's physiological role is largely unknown, because Mint germline knockouts are embryonic lethal. To analyze Mint/SHARP function in postnatal mice, we created Mint-floxed mice that allow the Cre/loxP-mediated conditional knockout of Mint. We analyzed Mint and RBP-J epistasis during Notch-dependent splenic B-lymphocyte development, and found that Mint suppresses Notch signaling through RBP-J. In addition, Mint deficiency caused severe hypoplasia in postnatal brain, suggesting it may regulate neuronal cell survival. genesis 45:300-306, 2007. (c) 2007 Wiley-Liss, Inc. |
