Factor XIII A-Subunit V34L Variant Affects Thrombus Cross-Linking in a Murine Model of Thrombosis | Zendy

Cédric Duval | Zendy; Majid Ali | Zendy; Waleed W. Chaudhry | Zendy; Victoria Ridger | Zendy; Robert A. S. Ariëns | Zendy; Helen Philippou | Zendy

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Factor XIII A-Subunit V34L Variant Affects Thrombus Cross-Linking in a Murine Model of Thrombosis

Author(s) -

Cédric Duval,

Majid Ali,

Waleed W. Chaudhry,

Victoria Ridger,

Robert A. S. Ariëns,

Helen Philippou

Publication year - 2016

Publication title -

arteriosclerosis thrombosis and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.115.306695

Subject(s) - fibrin , in vivo , recombinant dna , chemistry , thrombin , factor xiii , peptide , microbiology and biotechnology , thrombus , alanine , platelet activation , biochemistry , amino acid , biology , fibrinogen , immunology , platelet , medicine , gene

Factor XIII (FXIII) cross-links fibrin upon activation by thrombin. Activation involves cleavage at residue 37 by thrombin, releasing an activation peptide. A common polymorphism (valine to leucine variant at residue 34, V34L), located in the activation peptide, has been associated with increased activation rates and paradoxically a protective effect in cardiovascular disease. There is, currently, no data available on the effects of V34L from in vivo models of thrombosis. We examined the effect of FXIII V34L on clot formation and cross-linking in vivo.

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