| First Author | Michaelson JS | Year | 1999 |
| Journal | Genes Dev | Volume | 13 |
| Issue | 15 | Pages | 1918-23 |
| PubMed ID | 10444590 | Mgi Jnum | J:56796 |
| Mgi Id | MGI:1342427 | Doi | 10.1101/gad.13.15.1918 |
| Citation | Michaelson JS, et al. (1999) Loss of Daxx, a promiscuously interacting protein, results in extensive apoptosis in early mouse development. Genes Dev 13(15):1918-23 |
| abstractText | The mammalian Daxx gene has been identified in a diverse set of yeast interaction trap experiments. Although a facilitating role for Daxx in Fas-induced apoptosis has been suggested, Daxx's physiologic function remains unknown. To elucidate the in vivo role of Daxx, we have generated Daxx-deficient mice. Surprisingly, rather than a hyperproliferative disorder expected from the loss of a pro-apoptotic gene, mutation of Daxx results in extensive apoptosis and embryonic lethality. These findings argue against a role for Daxx in promoting Fas-induced cell death and suggest that Daxx either directly or indirectly suppresses apoptosis in the early embryo. |
