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神经变性疾病的定位及发病机制
(2007-11-10 19:52:55)
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健康/保健神经变性疾病定位发病机制翻译 |
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Location, Location, Location: Altered
Transcription Factor Trafficking in
Neurodegeneration
Chu, Charleen T. MD, PhD; Plowey, Edward D. MD,
PhD; Wang, Ying PhD; Patel, Vivek BA; Jordan-Sciutto, Kelly L.
PhD
Journal of Neuropathology & Experimental
Neurology. 66(10):873-883, October 2007.
Neurons may be particularly sensitive to
disruptions in transcription factor trafficking. Survival and
injury signals must traverse dendrites or axons, in addition to
soma, to affect nuclear transcriptional responses. Transcription
factors exhibit continued nucleocytoplasmic shuttling; the
predominant localization is regulated by binding to anchoring
proteins that mask nuclear localization/export signals and/or
target the factor for degradation. Two functional groups of
karyopherins, importins and exportins, mediate RanGTPase-dependent
transport through the nuclear pore. A growing number of recent
studies, in Alzheimer, Parkinson, and Lewy body diseases,
amyotrophic lateral sclerosis, and human immunodeficiency virus
encephalitis, implicate aberrant cytoplasmic localization of
transcription factors and their regulatory kinases in degenerating
neurons. Potential mechanisms include impaired nuclear import,
enhanced export, suppression of degradation, and sequestration in
protein aggregates or organelles and may reflect unmasking of
alternative cytoplasmic functions, both physiologic and pathologic.
Some "nuclear" factors also function in mitochondria, and importins
are also involved in axonal protein trafficking. Detrimental
consequences of a decreased nuclear to cytoplasmic balance include
suppression of neuroprotective transcription mediated by cAMP- and
electrophile/antioxidant-response elements and gain of toxic
cytoplasmic effects. Studying the pathophysiologic mechanisms
regulating transcription factor localization should facilitate
strategies to bypass deficits and restore adaptive neuroprotective
transcriptional responses.
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