Journal
DEVELOPMENTAL CELL
Volume 4, Issue 4, Pages 575-585Publisher
CELL PRESS
DOI: 10.1016/S1534-5807(03)00091-1
Keywords
-
Categories
Funding
- NIDCD NIH HHS [DC01919] Funding Source: Medline
- NINDS NIH HHS [NS38377, NS43691, NS37402, NS02130, NS18597, NS01849, R01 NS038932, NS34175, NS20020] Funding Source: Medline
Ask authors/readers for more resources
BAK is a pro-apoptotic BCL-2 family protein that localizes to mitochondria. Here we evaluate the function of BAK in several mouse models of neuronal injury including neuronotropic Sindbis virus infection, Parkinson's disease, ischemia/stroke, and seizure. BAK promotes or inhibits neuronal death depending on the specific death stimulus, neuron subtype, and stage of postnatal development. BAK protects neurons from excitotoxicity and virus infection in the hippocampus. As mice mature, BAK is converted from anti- to pro-death function in virus-infected spinal cord neurons. In addition to regulating cell death, BAK also protects mice from kainate-induced seizures, suggesting a possible role in regulating synaptic activity. BAK can alter neurotransmitter release in a direction consistent with its protective effects on neurons and mice. These findings suggest that BAK inhibits cell death by modifying neuronal excitability.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available