Abstract：
:The transcriptional co-activator p300 plays an important role in regulating gene expression in a number of different cell types. We have shown that wild type (WT) Presenilin 1 (PS1) stimulates the transcriptional activity ability of CREB Binding Protein (CBP), a close homolog of p300, whereas the Alzheimer's disease (AD) associated mutant of PS1 does not have this effect. A recent report has suggested that mutant PS1 can also disrupt the TCF/beta-catenin/CBP interaction but has no effect on the TCF/beta-catenin/p300 interaction. This suggests that the malregulation of CBP, but not of p300, caused by mutation in PS1 may be involved in the disease process. Here we show that wild type PS1 stimulates the transcriptional activity ability of p300 whereas an Alzheimer's disease-associated mutant of PS1 did not produce this effect. To our knowledge, this is the first report that shows regulation of p300 activity by WT PS1 and not by mutant PS1, indicating that like CBP, p300 can be differentially regulated by WT PS1 compared to its AD-associated mutant.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Francis YI,Diss JK,Kariti M,Stephanou A,Latchman DSdoi
10.1016/j.neulet.2006.11.036subject
Has Abstractpub_date
2007-02-14 00:00:00pages
137-40issue
2eissn
0304-3940issn
1872-7972pii
S0304-3940(06)01252-3journal_volume
413pub_type
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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pub_type： 杂志文章,评审
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
pub_type： 杂志文章
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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