| http://purl.uniprot.org/citations/16099885 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/16099885 | http://www.w3.org/2000/01/rdf-schema#comment | "High-throughput genomic technology identified an association between a single nucleotide polymorphism (SNP), a proline (P387) rather than the predominant alanine (A387) at position 387 in thrombospondin-4 (TSP-4) and premature myocardial infarction. The inflammatory hypothesis of atherosclerosis invokes a prominent role of leukocytes and cytokines in pathogenesis. As the expression of TSP-4 by vascular cells permits its exposure to circulating leukocytes, the interactions of human neutrophils (polymorphonuclear leukocytes [PMNs]) with both TSP-4 variants were investigated. Phorbol 12-myristate 13-acetate (PMA)-stimulated PMNs adhered and migrated well and equally on the TSP-4 variants. Integrin alpha(M)beta2 was identified as the TSP-4 receptor mediating these responses, and the 3 epidermal growth factor (EGF)-like domains of TSP-4 harboring the SNPs interacted with the alpha(M)I-domain. Despite the similarity in these responses, the P387 variant induced more robust tyrosine phosphorylation of the stress-related mitogen-activated protein kinases (MAPKs): p38MAPK and c-Jun NH2-terminal kinase (JNK), as well as signal transducer and activator of transcription-1 (STAT1) and heat shock protein 27 (HSP27) than the A387 variant. Additionally, cells adherent to P387 TSP-4 variant released 4-fold more H2O2 and secreted 2-fold more interleukin 8 (IL-8) as compared with the A387. H2O2 release and p38MAPK activation were totally inhibited by blockade of alpha(M)beta2. Thus, alpha(M)beta2 plays a central role in proinflammatory activities of TSP-4 (P387) and may contribute to the prothrombotic phenotype associated with this variant."xsd:string |
| http://purl.uniprot.org/citations/16099885 | http://purl.org/dc/terms/identifier | "doi:10.1182/blood-2005-03-1292"xsd:string |
| http://purl.uniprot.org/citations/16099885 | http://purl.uniprot.org/core/author | "Topol E.J."xsd:string |
| http://purl.uniprot.org/citations/16099885 | http://purl.uniprot.org/core/author | "Plow E.F."xsd:string |
| http://purl.uniprot.org/citations/16099885 | http://purl.uniprot.org/core/author | "Pluskota E."xsd:string |
| http://purl.uniprot.org/citations/16099885 | http://purl.uniprot.org/core/author | "Szpak D."xsd:string |
| http://purl.uniprot.org/citations/16099885 | http://purl.uniprot.org/core/author | "Krukovets I."xsd:string |
| http://purl.uniprot.org/citations/16099885 | http://purl.uniprot.org/core/author | "Stenina O.I."xsd:string |
| http://purl.uniprot.org/citations/16099885 | http://purl.uniprot.org/core/date | "2005"xsd:gYear |
| http://purl.uniprot.org/citations/16099885 | http://purl.uniprot.org/core/name | "Blood"xsd:string |
| http://purl.uniprot.org/citations/16099885 | http://purl.uniprot.org/core/pages | "3970-3978"xsd:string |
| http://purl.uniprot.org/citations/16099885 | http://purl.uniprot.org/core/title | "Mechanism and effect of thrombospondin-4 polymorphisms on neutrophil function."xsd:string |
| http://purl.uniprot.org/citations/16099885 | http://purl.uniprot.org/core/volume | "106"xsd:string |
| http://purl.uniprot.org/citations/16099885 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/16099885 |
| http://purl.uniprot.org/citations/16099885 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/16099885 |
| http://purl.uniprot.org/uniprot/P35443#attribution-EE17D26E5D4EAF8FFD85ABC84FA3FAB3 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/16099885 |