| http://purl.uniprot.org/citations/29777060 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/29777060 | http://www.w3.org/2000/01/rdf-schema#comment | "Although signaling of thrombin via its receptor protease-activated receptor 1 (Par1) is known to occur in atherothrombosis, its link to the actual pathogenesis of this condition is less clear. To better understand the role of thrombin-Par1 signaling in atherosclerosis, here we have studied their effects on cellular cholesterol efflux in mice. We found that by activating Par1 and cullin 3-mediated ubiquitination and degradation of ABC subfamily A member 1 (ABCA1), thrombin inhibits cholesterol efflux in both murine macrophages and smooth muscle cells. Moreover, disruption of the Par1 gene rescued ABCA1 from Western diet-induced ubiquitination and degradation and restored cholesterol efflux in apolipoprotein E-deficient (ApoE-/-) mice. Similarly, the Par1 deletion diminished diet-induced atherosclerotic lesions in the ApoE-/- mice. These observations for the first time indicate a role for thrombin-Par1 signaling in the pathogenesis of diet-induced atherosclerosis. We identify cullin 3 as a cullin-RING ubiquitin E3 ligase that mediates ABCA1 ubiquitination and degradation and thereby inhibits cholesterol efflux. Furthermore, compared with peripheral blood mononuclear cells (PBMCs) from ApoE-/- mice, the PBMCs from ApoE-/-:Par1-/- mice exhibited decreased trafficking to inflamed arteries of Western diet-fed ApoE-/- mice. This finding suggested that besides inhibiting cholesterol efflux, thrombin-Par1 signaling also plays a role in the recruitment of leukocytes during diet-induced atherogenesis. Based on these findings, we conclude that thrombin-Par1 signaling appears to contribute to the pathogenesis of atherosclerosis by impairing cholesterol efflux from cells and by recruiting leukocytes to arteries."xsd:string |
| http://purl.uniprot.org/citations/29777060 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.ra118.003491"xsd:string |
| http://purl.uniprot.org/citations/29777060 | http://purl.uniprot.org/core/author | "Raghavan S."xsd:string |
| http://purl.uniprot.org/citations/29777060 | http://purl.uniprot.org/core/author | "Singh N.K."xsd:string |
| http://purl.uniprot.org/citations/29777060 | http://purl.uniprot.org/core/author | "Rao G.N."xsd:string |
| http://purl.uniprot.org/citations/29777060 | http://purl.uniprot.org/core/author | "Mani A.M."xsd:string |
| http://purl.uniprot.org/citations/29777060 | http://purl.uniprot.org/core/date | "2018"xsd:gYear |
| http://purl.uniprot.org/citations/29777060 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/29777060 | http://purl.uniprot.org/core/pages | "10574-10589"xsd:string |
| http://purl.uniprot.org/citations/29777060 | http://purl.uniprot.org/core/title | "Protease-activated receptor 1 inhibits cholesterol efflux and promotes atherogenesis via cullin 3-mediated degradation of the ABCA1 transporter."xsd:string |
| http://purl.uniprot.org/citations/29777060 | http://purl.uniprot.org/core/volume | "293"xsd:string |
| http://purl.uniprot.org/citations/29777060 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/29777060 |
| http://purl.uniprot.org/citations/29777060 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/29777060 |
| http://purl.uniprot.org/uniprot/#_A0A1B0GX15-mappedCitation-29777060 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29777060 |
| http://purl.uniprot.org/uniprot/#_G3UWN5-mappedCitation-29777060 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29777060 |
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| http://purl.uniprot.org/uniprot/#_G3UZM8-mappedCitation-29777060 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29777060 |
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| http://purl.uniprot.org/uniprot/#_Q4FK40-mappedCitation-29777060 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29777060 |