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Caspase Regulation of Genotoxin-induced Neural Precursor Cell Death by Cleta D'Sa; Barbara J. Klocke; Francesco Cecconi; Tulia Lindsten; Craig B. Thompson; Stanley J. Korsmeyer; Richard A. Flavell; Kevin A. Roth is a Neuroscience article available to read on EtoBox.

What is Caspase Regulation of Genotoxin-induced Neural Precursor Cell Death about?

## Abstract Neural precursor cells (NPCs) critically regulate brain morphogenesis and recent studies have revealed an unexpectedly high frequency of NPC chromosomal abnormalities and apoptosis in the developing brain. We have shown previously that the apoptotic response of NPCs to genotoxic agents is dependent on p53 and caspase‐9, but not Bax or caspase‐3 expression. In this study, we found that NPCs deficient in Apaf‐1, or both the pro‐apoptotic multidomain Bcl‐2 family members Bax and Bak, were resistant to cytosine arabinoside and γ‐irradiation‐induced apoptosis. Inhibitors of gene transcription, protein translation, and caspase activity also blocked genotoxin‐induced NPC apoptosis. Although caspase‐3 and caspase‐6 were both cleaved in response to DNA damage, neither of these effector caspases was critical for apoptosis. Genotoxin‐induced NPC death was accompanied by the generation of reactive oxygen species and could be inhibited by several known antioxidants. Conversely, DNA damage‐induced reactive oxygen species generation was inhibited significantly by gene disruption of __p53__, __Apaf‐1__, or __caspase‐9__, and combined deficiency of Bax and Bak, but not by caspase‐3 or c

Who reads Caspase Regulation of Genotoxin-induced Neural Precursor Cell Death?

Author

Cleta D'Sa; Barbara J. Klocke; Francesco Cecconi; Tulia Lindsten; Craig B. Thompson; Stanley J. Korsmeyer; Richard A. Flavell; Kevin A. Roth

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0360-4012)

Published

2003

Language

EN

Field

Neuroscience (Life Sciences)