| http://purl.uniprot.org/citations/18544684 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/18544684 | http://www.w3.org/2000/01/rdf-schema#comment | "Second messenger-mediated inside-out activation of integrin alphaIIbbeta3 is a key step in platelet aggregation. We recently showed strongly impaired but not absent alphaIIbbeta3-mediated aggregation of CalDAG-GEFI-deficient platelets activated with various agonists. Here we further evaluated the roles of CalDAG-GEFI and protein kinase C (PKC) for alphaIIbbeta3 activation in platelets activated with a PAR4 receptor-specific agonist, GYPGKF (PAR4p). Compared with wild-type controls, platelets treated with the PKC inhibitor Ro31-8220 or CalDAG-GEFI-deficient platelets showed a marked defect in aggregation at low (< 1mM PAR4p) but not high PAR4p concentrations. Blocking of PKC function in CalDAG-GEFI-deficient platelets, how-ever, strongly decreased aggregation at all PAR4p concentrations, demonstrating that CalDAG-GEFI and PKC represent separate, but synergizing, pathways important for alphaIIbbeta3 activation. PAR4p-induced aggregation in the absence of CalDAG-GEFI required cosignaling through the Galphai-coupled receptor for ADP, P2Y12. Independent roles for CalDAG-GEFI and PKC/Galphai signaling were also observed for PAR4p-induced activation of the small GTPase Rap1, with CalDAG-GEFI mediating the rapid but reversible activation of this small GTPase. In summary, our study identifies CalDAG-GEFI and PKC as independent pathways leading to Rap1 and alphaIIbbeta3 activation in mouse platelets activated through the PAR4 receptor."xsd:string |
| http://purl.uniprot.org/citations/18544684 | http://purl.org/dc/terms/identifier | "doi:10.1182/blood-2008-02-139733"xsd:string |
| http://purl.uniprot.org/citations/18544684 | http://purl.uniprot.org/core/author | "Bergmeier W."xsd:string |
| http://purl.uniprot.org/citations/18544684 | http://purl.uniprot.org/core/author | "Wagner D.D."xsd:string |
| http://purl.uniprot.org/citations/18544684 | http://purl.uniprot.org/core/author | "Cifuni S.M."xsd:string |
| http://purl.uniprot.org/citations/18544684 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
| http://purl.uniprot.org/citations/18544684 | http://purl.uniprot.org/core/name | "Blood"xsd:string |
| http://purl.uniprot.org/citations/18544684 | http://purl.uniprot.org/core/pages | "1696-1703"xsd:string |
| http://purl.uniprot.org/citations/18544684 | http://purl.uniprot.org/core/title | "CalDAG-GEFI and protein kinase C represent alternative pathways leading to activation of integrin alphaIIbbeta3 in platelets."xsd:string |
| http://purl.uniprot.org/citations/18544684 | http://purl.uniprot.org/core/volume | "112"xsd:string |
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| http://purl.uniprot.org/uniprot/#_D3Z2F9-mappedCitation-18544684 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18544684 |
| http://purl.uniprot.org/uniprot/#_D3YXD6-mappedCitation-18544684 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18544684 |
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| http://purl.uniprot.org/uniprot/#_D6RDD3-mappedCitation-18544684 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18544684 |
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| http://purl.uniprot.org/uniprot/#_D3YZP4-mappedCitation-18544684 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18544684 |
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| http://purl.uniprot.org/uniprot/#_O54890-mappedCitation-18544684 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18544684 |