Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2010-4-27
pubmed:abstractText
Toll-like receptors (TLRs) and the scavenger receptor CD36 are key molecular sensors for the innate immune response to invading pathogens. However, these receptors may also recognize endogenous "danger signals" generated during brain injury, such as cerebral ischemia, and trigger a maladaptive inflammatory reaction. Indeed, CD36 and TLR2 and 4 are involved in the inflammation and related tissue damage caused by brain ischemia. Because CD36 may act as a coreceptor for TLR2 heterodimers (TLR2/1 or TLR2/6), we tested whether such interaction plays a role in ischemic brain injury.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1524-4628
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
41
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
898-904
pubmed:dateRevised
2010-12-3
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Key role of CD36 in Toll-like receptor 2 signaling in cerebral ischemia.
pubmed:affiliation
Division of Neurobiology, Weill Cornell Medical College, 407 E 61st St, Room RR303, New York, NY 10065, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, N.I.H., Extramural