Bax limits adult neural stem cell persistence through caspase and IP3 receptor activation

摘要: Neural stem cells in the mammalian brain persist and are functional well into adulthood. There is, however, little insight mechanisms that control adult neural cell survival. Mice deficient proapoptotic molecule Bax exhibit increased numbers of multipotent progenitor subventricular zone. In vitro, these progenitors behave as utilize caspase activation to direct death. We demonstrate predominate mechanism underlying Bax-mediated death lies modulation calcium flux through interaction with IP3 receptor.