Linked Life Data

21817106

Source:http://linkedlifedata.com/resource/pubmed/id/21817106

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2011-8-18
pubmed:abstractText
Deletion of the mitochondrial gene p66(Shc) protects from endothelial dysfunction and atherosclerotic plaque formation in mice fed a high-fat diet. However, the molecular mechanisms underlying this beneficial effect have not yet been delineated. The present study was designed to elucidate the proatherogenic mechanisms by which p66(Shc) mediates oxidized low-density lipoprotein (oxLDL) uptake by the endothelium, a critical step in plaque formation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1524-4636
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2090-7
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Oxidized low-density lipoprotein activates p66Shc via lectin-like oxidized low-density lipoprotein receptor-1, protein kinase C-beta, and c-Jun N-terminal kinase kinase in human endothelial cells.
pubmed:affiliation
Cardiovascular Research, Institute of Physiology, University of Zürich, Zürich, Switzerland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't