Linked Life Data

18617174

Source:http://linkedlifedata.com/resource/pubmed/id/18617174

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-1-26
pubmed:abstractText
Outward arterial remodeling is a structural enlargement of the artery that is associated with unstable inflammatory atherosclerotic lesions. Toll-like receptor (Tlr) activation is known as a key pathway in outward arterial remodeling. Tlr activation results in nuclear translocation of the transcription factor Nuclear Factor-kappa B (NF-kappaB) that controls the transcription of many inflammatory genes. The NF-kappaB subunit p50 is generally considered to be an inhibitory subunit of the NF-kappaB complex. We therefore hypothesize that NF-kappaB p50 inhibits outward arterial remodeling.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1879-1484
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
202
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
424-30
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
The Nuclear Factor-kappa B p50 subunit is involved in flow-induced outward arterial remodeling.
pubmed:affiliation
Department Experimental Cardiology, University Medical Center Utrecht, The Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't