| http://purl.uniprot.org/citations/12218060 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/12218060 | http://www.w3.org/2000/01/rdf-schema#comment | "The endothelial cell protein C receptor (EPCR) is a type 1 transmembrane protein found primarily on endothelium that binds both protein C and activated protein C with similar affinity. EPCR augments the activation of protein C by the thrombin-thrombomodulin complex. To determine the physiological importance of EPCR, we generated EPCR-deficient mice by homologous targeting in embryonic stem cells. Genotyping of progeny obtained from EPCR(+/-) interbreeding indicated that EPCR(-/-) embryos died on or before embryonic day 10.5 (E10.5). Reverse transcriptase-PCR confirmed the absence of EPCR mRNA in EPCR(-/-) embryos. EPCR(-/-) embryos removed from extra-embryonic membranes and tissues at day E7.5 and cultured in vitro developed beyond E10.5, suggesting a role for EPCR in the normal function of the placenta and/or at the materno-embryonic interface. Immunohistochemistry revealed the lack of EPCR in trophoblast giant cells of EPCR(-/-) embryos. These cells, which normally express EPCR, are in direct contact with the maternal circulation and its clotting factors. In EPCR(-/-) embryos, greatly increased fibrin deposition was detected around these cells. To prevent this fibrin deposition, EPCR(+/-)-crossed female mice received a daily subcutaneous injection of enoxaparin through pregnancy. Although some EPCR(-/-) embryos were rescued from midgestational lethality, this regimen yielded no EPCR(-/-) pups. We conclude that EPCR is essential for normal embryonic development. Moreover, EPCR plays a key role in preventing thrombosis at the maternal-embryonic interface."xsd:string |
| http://purl.uniprot.org/citations/12218060 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m207538200"xsd:string |
| http://purl.uniprot.org/citations/12218060 | http://purl.uniprot.org/core/author | "Li W."xsd:string |
| http://purl.uniprot.org/citations/12218060 | http://purl.uniprot.org/core/author | "Zhang F."xsd:string |
| http://purl.uniprot.org/citations/12218060 | http://purl.uniprot.org/core/author | "Crawley J.T."xsd:string |
| http://purl.uniprot.org/citations/12218060 | http://purl.uniprot.org/core/author | "Esmon C.T."xsd:string |
| http://purl.uniprot.org/citations/12218060 | http://purl.uniprot.org/core/author | "Gu J.M."xsd:string |
| http://purl.uniprot.org/citations/12218060 | http://purl.uniprot.org/core/author | "Esmon N.L."xsd:string |
| http://purl.uniprot.org/citations/12218060 | http://purl.uniprot.org/core/author | "Ferrell G."xsd:string |
| http://purl.uniprot.org/citations/12218060 | http://purl.uniprot.org/core/date | "2002"xsd:gYear |
| http://purl.uniprot.org/citations/12218060 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/12218060 | http://purl.uniprot.org/core/pages | "43335-43343"xsd:string |
| http://purl.uniprot.org/citations/12218060 | http://purl.uniprot.org/core/title | "Disruption of the endothelial cell protein C receptor gene in mice causes placental thrombosis and early embryonic lethality."xsd:string |
| http://purl.uniprot.org/citations/12218060 | http://purl.uniprot.org/core/volume | "277"xsd:string |
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