Source:http://linkedlifedata.com/resource/pubmed/id/17984683
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
11
|
| pubmed:dateCreated |
2007-11-6
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| pubmed:abstractText |
Impaired transduction of transforming growth factor-beta signaling has recently been implicated in Alzheimer disease. Transforming growth factor-beta signals are transduced by Smads, which are phosphorylated and translocated to the nucleus, where they initiate gene transcription. In Alzheimer disease, neurofibrillary tangles sequester phosphorylated Smad 2/3 (pSmad2/3) and reduce its nuclear translocation. We have now investigated the relationship between pSmad2/3 and phospho-tau in 3 other tauopathies, Pick disease, progressive supranuclear palsy, and corticobasal degeneration, and in 2 alpha-synucleinopathies, dementia with Lewy bodies and multiple system atrophy. In Pick disease, progressive supranuclear palsy, and corticobasal degeneration, pSmad2/3 was demonstrated in neuronal and glial nuclei but also colocalized with cytoplasmic tau inclusions. No pSmad2/3 was detected in glial cytoplasmic inclusions in multiple system atrophy or in Lewy bodies in dementia with Lewy bodies. Our data indicate that phospho-tau but not alpha-synuclein cytoplasmic inclusions bind pSmad2/3. The preservation of neuronal nuclear pSmad2/3 in Pick disease, progressive supranuclear palsy, and corticobasal degeneration suggests that cytoplasmic sequestration of pSmad2/3 is likely to have less impact on transforming growth factor-beta signal transduction in these diseases than in Alzheimer disease.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Nov
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| pubmed:issn |
0022-3069
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
66
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1019-26
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| pubmed:meshHeading |
pubmed-meshheading:17984683-Aged,
pubmed-meshheading:17984683-Aged, 80 and over,
pubmed-meshheading:17984683-Blotting, Western,
pubmed-meshheading:17984683-Brain,
pubmed-meshheading:17984683-Female,
pubmed-meshheading:17984683-Fluorescent Antibody Technique,
pubmed-meshheading:17984683-Humans,
pubmed-meshheading:17984683-Immunohistochemistry,
pubmed-meshheading:17984683-Inclusion Bodies,
pubmed-meshheading:17984683-Lewy Body Disease,
pubmed-meshheading:17984683-Male,
pubmed-meshheading:17984683-Multiple System Atrophy,
pubmed-meshheading:17984683-Neurodegenerative Diseases,
pubmed-meshheading:17984683-Phosphorylation,
pubmed-meshheading:17984683-Pick Disease of the Brain,
pubmed-meshheading:17984683-Protein Transport,
pubmed-meshheading:17984683-Smad Proteins,
pubmed-meshheading:17984683-Supranuclear Palsy, Progressive,
pubmed-meshheading:17984683-alpha-Synuclein,
pubmed-meshheading:17984683-tau Proteins
|
| pubmed:year |
2007
|
| pubmed:articleTitle |
Phosphorylated Smad 2/3 colocalizes with phospho-tau inclusions in Pick disease, progressive supranuclear palsy, and corticobasal degeneration but not with alpha-synuclein inclusions in multiple system atrophy or dementia with Lewy bodies.
|
| pubmed:affiliation |
Dementia Research Group, University of Bristol Institute of Clinical Neurosciences, Department of Clinical Science at North Bristol, Frenchay Hospital, Bristol, BS16 1LE, UK.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|