Abstract：
:Amyotrophic lateral sclerosis (ALS) is a progressive and fatal disease caused by the selective death of motor neurons. Between 5% and 10% of ALS patients have a genetically inherited form of the disease known as familial ALS (FALS), and approximately 20% of FALS patients have mutations in the SOD1 gene. Although the mechanism underlying motor neuron death has not yet been fully clarified, it is supposed to be not completely consistent with apoptosis, necrosis, or autophagic cell death. Recently, it was found that general transcriptional repression induces slowly progressive atypical cell death associated with the shift of balance between YAPdeltaCs as prosurvival factors and activated p73 promoting apoptosis. This type of neuronal death was named transcriptional repression-induced atypical death (TRIAD). Therefore, to investigate possible relationships between the mechanism of motor neuron death in ALS and TRIAD, G93ASOD1 transgenic mice (Tg) were examined as an ALS model. The levels of YAPdeltaCs in the spinal cords of Tg mice decreased with disease progression, even during the presymptomatic stage, whereas FL-YAP, a p73 cofactor that promotes apoptosis, was preserved until the late symptomatic stage. Although the expression of total p73 also decreased with age in Tg mice, the ratio of phosphorylated p73 to total p73 increased during the late symptomatic stage in Tg mice. These results suggest that the progressive decrease in the levels of YAPdeltaCs and the relative increase in phosphorylation of p73 over the time course are correlated with disease progression in ALS model animals.
journal_name
J Neurosci Resjournal_title
Journal of neuroscience researchauthors
Morimoto N,Nagai M,Miyazaki K,Kurata T,Takehisa Y,Ikeda Y,Kamiya T,Okazawa H,Abe Kdoi
10.1002/jnr.21902subject
Has Abstractpub_date
2009-03-01 00:00:00pages
928-36issue
4eissn
0360-4012issn
1097-4547journal_volume
87pub_type
杂志文章abstract：:We describe here a novel monoclonal antibody (mab H6) which recognizes CD9, an integral cell surface constituent previously described in cells of the hematopoietic lineage and involved in the aggregation of platelets. Mab H6 was raised against membranes of immature mouse astrocytes and reacted with a protein of 25-27 ...
journal_title：Journal of neuroscience research
pub_type： 杂志文章
doi：10.1002/jnr.490430103
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journal_title：Journal of neuroscience research
pub_type： 杂志文章
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pub_type： 杂志文章
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journal_title：Journal of neuroscience research
pub_type： 杂志文章
doi：10.1002/jnr.490330107
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pub_type： 杂志文章
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journal_title：Journal of neuroscience research
pub_type： 杂志文章,评审
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journal_title：Journal of neuroscience research
pub_type： 杂志文章
doi：10.1002/jnr.24054
更新日期：2018-04-01 00:00:00
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journal_title：Journal of neuroscience research
pub_type： 杂志文章
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journal_title：Journal of neuroscience research
pub_type： 杂志文章
doi：10.1002/jnr.21854
更新日期：2009-02-01 00:00:00
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journal_title：Journal of neuroscience research
pub_type： 杂志文章
doi：10.1002/jnr.20626
更新日期：2005-11-01 00:00:00
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journal_title：Journal of neuroscience research
pub_type： 杂志文章
doi：10.1002/jnr.490320108
更新日期：1992-05-01 00:00:00
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journal_title：Journal of neuroscience research
pub_type： 杂志文章
doi：10.1002/jnr.20743
更新日期：2006-03-01 00:00:00
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journal_title：Journal of neuroscience research
pub_type： 杂志文章
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pub_type： 杂志文章
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更新日期：1981-01-01 00:00:00
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journal_title：Journal of neuroscience research
pub_type： 杂志文章
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更新日期：1997-07-01 00:00:00
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更新日期：2004-08-01 00:00:00
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journal_title：Journal of neuroscience research
pub_type： 杂志文章
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pub_type： 杂志文章
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