BAK alters neuronal excitability and can switch from anti- to pro-death function during postnatal development

Title
BAK alters neuronal excitability and can switch from anti- to pro-death function during postnatal development
Authors
김종현Yihru FannjiangRichard L. HuganirShifa ZouTullia LindstenCraig B. ThompsonToshiaki MitoRichard J. TraystmanThomas LarsenDiane E. GriffinAllen S. MandirTed M. DawsonSonny DikeAndrea L. SappingtonDouglas A. KerrElizabeth A. JonasLeonard K. KaczmarekJ. Marie Hardwick
Issue Date
2003-04
Publisher
Developmental cell
Citation
VOL 4, NO 4, 575-585
Abstract
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.
URI
http://pubs.kist.re.kr/handle/201004/59178
ISSN
15345807
Appears in Collections:
KIST Publication > Article
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