Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18
pubmed:dateCreated
2004-11-2
pubmed:abstractText
Enhanced production of reactive oxygen species (ROS) has been recognized as the major determinant of age-related endothelial dysfunction. The p66shc protein controls cellular responses to oxidative stress. Mice lacking p66shc (p66shc-/-) have increased resistance to ROS and a 30% prolonged life span. The present study investigates age-dependent changes of endothelial function in this model.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/3-nitrotyrosine, http://linkedlifedata.com/resource/pubmed/chemical/Adaptor Proteins, Signal Transducing, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type III, http://linkedlifedata.com/resource/pubmed/chemical/Nos2 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Nos3 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Reactive Oxygen Species, http://linkedlifedata.com/resource/pubmed/chemical/Shc Signaling Adaptor Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Shc1 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Superoxide Dismutase, http://linkedlifedata.com/resource/pubmed/chemical/Tyrosine
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1524-4539
pubmed:author
pubmed:issnType
Electronic
pubmed:day
2
pubmed:volume
110
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2889-95
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:15505103-Adaptor Proteins, Signal Transducing, pubmed-meshheading:15505103-Aging, pubmed-meshheading:15505103-Animals, pubmed-meshheading:15505103-Aorta, pubmed-meshheading:15505103-Endothelium, Vascular, pubmed-meshheading:15505103-Isometric Contraction, pubmed-meshheading:15505103-Longevity, pubmed-meshheading:15505103-Male, pubmed-meshheading:15505103-Mice, pubmed-meshheading:15505103-Mice, Knockout, pubmed-meshheading:15505103-Nitric Oxide, pubmed-meshheading:15505103-Nitric Oxide Synthase, pubmed-meshheading:15505103-Nitric Oxide Synthase Type II, pubmed-meshheading:15505103-Nitric Oxide Synthase Type III, pubmed-meshheading:15505103-Oxidative Stress, pubmed-meshheading:15505103-Proteins, pubmed-meshheading:15505103-Reactive Oxygen Species, pubmed-meshheading:15505103-Shc Signaling Adaptor Proteins, pubmed-meshheading:15505103-Superoxide Dismutase, pubmed-meshheading:15505103-Tyrosine, pubmed-meshheading:15505103-Vasoconstriction
pubmed:year
2004
pubmed:articleTitle
Deletion of p66shc gene protects against age-related endothelial dysfunction.
pubmed:affiliation
Cardiovascular Research & Cardiology, Institute of Physiology, Zürich, Irchel and University Hospital, Zürich, Switzerland.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't