Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2008-12-24
pubmed:abstractText
The mitogen-activated protein (MAP) kinases ERK2, p38 and JNK1 are present in platelets and are activated by various stimuli, such as thrombin, collagen, von Willebrand factor (VWF) and ADP. Until recently, MAP kinases were only studied in the conventional model of agonist-induced platelet aggregation mediated by fibrinogen and integrin alphaIIbbeta3. However, this approach is likely to be too limited for a physiological understanding of platelet MAP kinases and their signaling pathways. Recent studies with varying blood-flow conditions and animal models of thrombosis have provided deeper insight into the role of MAP kinases in thrombus formation and the dependence of these kinases on shear conditions. This review summarizes and discusses the physiological functions of these kinases in hemostasis and thrombosis as revealed by various technical approaches.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1538-7836
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2007-16
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Mitogen-activated protein kinases in hemostasis and thrombosis.
pubmed:affiliation
Centre de Recherche Cardiovasculaire INSERM Lariboisiére U689, Hôpital Lariboisiére, Paris, France.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't