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A novel mutation in the P2Y12 receptor and a function-reducing polymorphism in protease-activated receptor 1 in a patient with chronic bleeding.
Patel, Y M; Lordkipanidzé, M; Lowe, G C; Nisar, S P; Garner, K; Stockley, J; Daly, M E; Mitchell, M; Watson, S P; Austin, S K; Mundell, S J.
Afiliación
  • Patel YM; Department of Cardiology, Cardiovascular Division, King's College London, The Rayne Institute, St Thomas' Hospital, London, UK.
J Thromb Haemost ; 12(5): 716-25, 2014 May.
Article en En | MEDLINE | ID: mdl-24612435
BACKGROUND: The study of patients with bleeding problems is a powerful approach in determining the function and regulation of important proteins in human platelets. We have identified a patient with a chronic bleeding disorder expressing a homozygous P2RY(12) mutation, predicting an arginine to cysteine (R122C) substitution in the G-protein-coupled P2Y(12) receptor. This mutation is found within the DRY motif, which is a highly conserved region in G-protein-coupled receptors (GPCRs) that is speculated to play a critical role in regulating receptor conformational states. OBJECTIVES: To determine the functional consequences of the R122C substitution for P2Y(12) function. PATIENT/METHODS: We performed a detailed phenotypic analysis of an index case and affected family members. An analysis of the variant R122C P2Y(12) stably expressed in cells was also performed. RESULTS: ADP-stimulated platelet aggregation was reduced as a result of a significant impairment of P2Y(12) activity in the patient and family members. Cell surface R122C P2Y(12) expression was reduced both in cell lines and in platelets; in cell lines, this was as a consequence of agonist-independent internalization followed by subsequent receptor trafficking to lysosomes. Strikingly, members of this family also showed reduced thrombin-induced platelet activation, owing to an intronic polymorphism in the F2R gene, which encodes protease-activated receptor 1 (PAR-1), that has been shown to be associated with reduced PAR-1 receptor activity. CONCLUSIONS: Our study is the first to demonstrate a patient with deficits in two stimulatory GPCR pathways that regulate platelet activity, further indicating that bleeding disorders constitute a complex trait.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Polimorfismo Genético / Plaquetas / Receptor PAR-1 / Receptores Purinérgicos P2Y12 / Hemorragia / Mutación Tipo de estudio: Prognostic_studies Límite: Female / Humans / Male Idioma: En Revista: J Thromb Haemost Asunto de la revista: HEMATOLOGIA Año: 2014 Tipo del documento: Article Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Polimorfismo Genético / Plaquetas / Receptor PAR-1 / Receptores Purinérgicos P2Y12 / Hemorragia / Mutación Tipo de estudio: Prognostic_studies Límite: Female / Humans / Male Idioma: En Revista: J Thromb Haemost Asunto de la revista: HEMATOLOGIA Año: 2014 Tipo del documento: Article Pais de publicación: Reino Unido