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<a href="http://doi.org/10.1111/j.1471-4159.2004.02834.x" target="_blank" rel="noreferrer noopener">http://doi.org/10.1111/j.1471-4159.2004.02834.x</a>
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Pages
59-71
Issue
1
Volume
92
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Title
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RNAi knockdown of Par-4 inhibits neurosynaptic degeneration in ALS-linked mice
Publisher
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Journal of Neurochemistry
Date
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2005
2005-01
Subject
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amyotrophic lateral sclerosis; amyotrophic lateral sclerosis; anterior horn; antisense oligonucleotides; apoptosis; apoptosis response-4; Biochemistry & Molecular Biology; cells; Cu/Zn superoxide dismutase; motor-neuron degeneration; neurons; Neurosciences & Neurology; prostate; protein; RNA interference; sod1; spinal motor neurons; synapse; synapses; transgenic mouse model
Creator
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Xie J; Awad K S; Guo Q
Description
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Evidence from human amyotrophic lateral sclerosis (ALS) patients and ALS-linked Cu/Zn superoxide dismutase (Cu/Zn-SOD) transgenic mice bearing the mutation of glycine to alanine at position 93 (G93A) suggests that the pro-apoptotic protein prostate apoptosis response-4 (Par-4) might be a critical link in the chain of events leading to motor neuron degeneration. We now report that Par-4 is enriched in synaptosomes and post-synaptic density from the ventral horn of the spinal cord. Levels of Par-4 in synaptic compartments increased significantly during rapid and slow declining stages of muscle strength in hSOD1 G93A mutant mice. In the pre-muscle weakness stage, hSOD1 G93A mutation sensitized synaptosomes from the ventral horn of the spinal cord to increased levels of Par-4 expression following excitotoxic and apoptotic insults. In ventral spinal synaptosomes, Par-4-mediated production of pro-apoptotic cytosolic factor(s) was significantly enhanced by the hSOD1 G93A mutation. RNA interference (RNAi) knockdown of Par-4 inhibited mitochondrial dysfunction and caspase-3 activation induced by G93A mutation in synaptosomes from the ventral horn of the spinal cord, and protected spinal motor neurons from apoptosis. These results identify the synapse as a crucial cellular site for the cell death promoting actions of Par-4 in motor neurons, and suggest that targeted inhibition of Par-4 by RNAi may prove to be a neuroprotective strategy for motor neuron degeneration.
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<a href="http://doi.org/10.1111/j.1471-4159.2004.02834.x" target="_blank" rel="noreferrer noopener">10.1111/j.1471-4159.2004.02834.x</a>
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Journal Article
2005
amyotrophic lateral sclerosis
anterior horn
antisense oligonucleotides
Apoptosis
apoptosis response-4
Awad K S
Biochemistry & Molecular Biology
Cells
Cu/Zn superoxide dismutase
Guo Q
Journal Article
Journal of neurochemistry
motor-neuron degeneration
Neurons
Neurosciences & Neurology
Prostate
Protein
RNA Interference
sod1
spinal motor neurons
synapse
synapses
transgenic mouse model
Xie J