Abstract
Bax is a pro-apoptotic Bcl-2 family protein that regulates programmed cell death through homodimerization and through heterodimerization with Bcl-2. Bax α is encoded by six exons and undergoes alternative splicing. Bax κ, a splice variant of Bax with conserved BH1, BH2 and BH3 binding domains and a C-terminal transmembrane domain (TM), but with an extra 446-bp insert between exons 1 and 2 leading to loss of an N-terminal ART domain, was identified from an ischemic rat brain cDNA library. Expression of Bax κ mRNA and protein was up-regulated in hippocampus after cerebral ischemic injury. The increased Bax κ mRNA was distributed mainly in selectively vulnerable hippocampal CA1 neurons that are destined to die after global ischemia. Overexpression of Bax κ protein in HN33 mouse hippocampal neuronal cells induced cell death, which was partially abrogated by co-overexpression of Bcl-2. Moreover, co-overexpression of Bax κ and Bax α increased HN33 cell death. The results suggest that the Bax κ may have a role in ischemic neuronal death.
Original language | English |
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Pages (from-to) | 1508-1519 |
Number of pages | 12 |
Journal | Journal of Neurochemistry |
Volume | 77 |
Issue number | 6 |
DOIs | |
State | Published - 2001 |
Keywords
- Bax
- Cerebral ischemia
- Gene expression
- Neuron
- Programmed cell death