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

J. Shi, L. F. Parada, Steven G. Kernie

Research output: Contribution to journalArticlepeer-review

23 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1601-1612
Number of pages12
JournalCell Death and Differentiation
Volume12
Issue number12
DOIs
StatePublished - Dec 2005

Keywords

  • Adult neural stem cells
  • Apoptosis
  • Calcium
  • Caspase-3
  • IP3 receptor
  • Subventricular zone

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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