Linked Life Data

17099291

Source:http://linkedlifedata.com/resource/pubmed/id/17099291

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-11-22
pubmed:abstractText
Presenilin 1 (PS1) is a multifunctional protein, and its mutations are highly related to familial Alzheimer's disease (AD). In this study, we examined the effects of PS1 overexpression on neuronal morphology using SH-SY5Y cells. Overexpression of dominant-negative D385A PS1 induced morphological change and impairment of neurite formation, while those of wild-type and pathogenic P117L mutant PS1 did not change cellular morphology compared with native cells. Moreover, filopodium-formation-related proteins were decreased only in cells overexpressing D385A PS1. Therefore, PS1 may be involved in neuritogenesis and morphological change in SH-SY5Y cells, and P117L mutation may linked to AD by different mechanisms.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1347-8613
pubmed:author
pubmed:issnType
Print
pubmed:volume
102
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
354-8
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Morphological change by overexpression of D385A dominant negative presenilin 1 in human neuroblastoma SH-SY5Y cells.
pubmed:affiliation
Department of Neurobiology and 21st Century COE Program, Kyoto Pharmaceutical University, Kyoto, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't