| pubmed-article:15943976 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15943976 | lifeskim:mentions | umls-concept:C0003280 | lld:lifeskim |
| pubmed-article:15943976 | lifeskim:mentions | umls-concept:C0033621 | lld:lifeskim |
| pubmed-article:15943976 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:15943976 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:15943976 | pubmed:issue | 15 | lld:pubmed |
| pubmed-article:15943976 | pubmed:dateCreated | 2005-6-9 | lld:pubmed |
| pubmed-article:15943976 | pubmed:abstractText | The anticoagulant protein C system regulates the activity of coagulation factors VIIIa and Va, cofactors in the activation of factor X and prothrombin, respectively. Protein C is activated on endothelium by the thrombin-thrombomodulin-EPCR (endothelial protein C receptor) complex. Activated protein C (APC)-mediated cleavages of factors VIIIa and Va occur on negatively charged phospholipid membranes and involve protein cofactors, protein S and factor V. APC also has anti-inflammatory and anti-apoptotic activities that involve binding of APC to EPCR and cleavage of PAR-1 (protease-activated receptor-1). Genetic defects affecting the protein C system are the most common risk factors of venous thrombosis. The protein C system contains multi-domain proteins, the molecular recognition of which will be reviewed. | lld:pubmed |
| pubmed-article:15943976 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15943976 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15943976 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15943976 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:15943976 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15943976 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:15943976 | pubmed:issn | 0014-5793 | lld:pubmed |
| pubmed-article:15943976 | pubmed:author | pubmed-author:VilloutreixBr... | lld:pubmed |
| pubmed-article:15943976 | pubmed:author | pubmed-author:DahlbäckBjörn... | lld:pubmed |
| pubmed-article:15943976 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15943976 | pubmed:day | 13 | lld:pubmed |
| pubmed-article:15943976 | pubmed:volume | 579 | lld:pubmed |
| pubmed-article:15943976 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15943976 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15943976 | pubmed:pagination | 3310-6 | lld:pubmed |
| pubmed-article:15943976 | pubmed:dateRevised | 2005-11-16 | lld:pubmed |
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| pubmed-article:15943976 | pubmed:meshHeading | pubmed-meshheading:15943976... | lld:pubmed |
| pubmed-article:15943976 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15943976 | pubmed:articleTitle | The anticoagulant protein C pathway. | lld:pubmed |
| pubmed-article:15943976 | pubmed:affiliation | Department of Laboratory Medicine, Clinical Chemistry, Lund University, The Wallenberg laboratory, University Hospital, Malmö, SE-205 02 Malmö, Sweden. bjorn.dahlback@klkemi.mas.lu.se | lld:pubmed |
| pubmed-article:15943976 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15943976 | pubmed:publicationType | Review | lld:pubmed |
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