Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2003-10-13
pubmed:abstractText
Neointima formation occurs in arteries in response to mechanical or chemical injury and is responsible for substantial morbidity. In this work, the role of the intracellular linker protein Grb2 in the pathogenesis of neointima formation was examined. Grb2 is a critical signaling protein that facilitates the activation of the small GTPase ras by receptor tyrosine kinases.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1524-4636
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1788-93
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:12842846-Adaptor Proteins, Signal Transducing, pubmed-meshheading:12842846-Animals, pubmed-meshheading:12842846-Aorta, pubmed-meshheading:12842846-Arteriosclerosis, pubmed-meshheading:12842846-Carotid Arteries, pubmed-meshheading:12842846-Carotid Artery Injuries, pubmed-meshheading:12842846-Cell Division, pubmed-meshheading:12842846-Cells, Cultured, pubmed-meshheading:12842846-Disease Models, Animal, pubmed-meshheading:12842846-GRB2 Adaptor Protein, pubmed-meshheading:12842846-Mice, pubmed-meshheading:12842846-Mice, Knockout, pubmed-meshheading:12842846-Muscle, Smooth, Vascular, pubmed-meshheading:12842846-Proteins, pubmed-meshheading:12842846-Rats, pubmed-meshheading:12842846-Signal Transduction, pubmed-meshheading:12842846-Tunica Intima, pubmed-meshheading:12842846-Vascular Diseases
pubmed:year
2003
pubmed:articleTitle
Grb2 is required for the development of neointima in response to vascular injury.
pubmed:affiliation
Center for Cardiovascular Research, Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't