| First Author | Shi J | Year | 2005 |
| Journal | Cell Death Differ | Volume | 12 |
| Issue | 12 | Pages | 1601-12 |
| PubMed ID | 15947791 | Mgi Jnum | J:116534 |
| Mgi Id | MGI:3694443 | Doi | 10.1038/sj.cdd.4401676 |
| Citation | Shi J, et al. (2005) Bax limits adult neural stem cell persistance through caspase and IP3 receptor activation. Cell Death Differ 12(12):1601-1612 |
| abstractText | Neural stem cells in the mammalian brain persist and are functional well into adulthood. There is, however, little insight into mechanisms that control adult neural stem cell survival. Mice deficient in the proapoptotic molecule Bax exhibit increased numbers of multipotent progenitor cells in the adult subventricular zone. In vitro, these progenitors behave as neural stem cells and utilize Bax and caspase activation to direct cell death. We demonstrate that the predominate mechanism underlying caspase and Bax-mediated adult neural stem cell death lies in the modulation of calcium flux through interaction with the IP3 receptor. |
