Linked Life Data

19372457

Source:http://linkedlifedata.com/resource/pubmed/id/19372457

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2009-6-18
pubmed:abstractText
Several findings argue for a protective effect of high-density lipoproteins (HDLs) against endothelial dysfunction. The molecular mechanisms underlying this protective effect are not fully understood, although recent works suggest that the actions of HDL on the endothelium are initiated by multiple interactions between HDLs (lipid or protein moiety) and cell surface receptors. We previously showed that the mitochondrial related F(1)-ATPase is a cell surface receptor for HDLs and their main atheroprotective apolipoprotein (apoA-I). Herein we test the hypothesis that the cell surface F(1)-ATPase may contribute to the ability of apoA-I and HDLs to maintain endothelial cell survival.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1524-4636
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1125-30
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Stimulation of cell surface F1-ATPase activity by apolipoprotein A-I inhibits endothelial cell apoptosis and promotes proliferation.
pubmed:affiliation
INSERM U563, Département Lipoprotéines et Médiateurs Lipidiques, Toulouse, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't