Linked Life Data

15811328

Source:http://linkedlifedata.com/resource/pubmed/id/15811328

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2005-4-6
pubmed:abstractText
Insoluble deposits of tau and amyloid precursor protein (APP) peptides Abeta characterize Alzheimer's disease. We studied the role of tau in the metabolism of APP in cells stably expressing APP Swedish mutation (CHOsw). Transient expression of tau in CHOsw cells caused morphological changes, bundling of microtubules and perinuclear aggregation of Golgi-derived vesicles. It also reduced the secretion of Abeta(1-40) and Abeta(1-42) without altering the APP steady state levels. This was accompanied by a reduction in the gamma-secretase and an increase in the insulin degrading enzyme activities. Our results suggest that tau may play an inhibitory role in the amyloidogenic activity of APP.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0014-5793
pubmed:author
pubmed:issnType
Print
pubmed:day
11
pubmed:volume
579
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2119-24
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Expression of tau reduces secretion of Abeta without altering the amyloid precursor protein content in CHOsw cells.
pubmed:affiliation
Neuroinflammation Research Laboratories, Department of Psychiatry of the Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't