title: In silico analysis highlights the copy number variation mechanism responsible for the historically reported VWF exon 42 deletion.
authors.affiliation: Haemostasis Research Group, Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, UK.
authors.forename: A
authors.initials: A
authors.lastname: Cartwright
authors.affiliation: Haemostasis Research Group, Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, UK.
authors.forename: I R
authors.initials: IR
authors.lastname: Peake
authors.affiliation: Haemostasis Research Group, Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, UK.
authors.forename: A C
authors.identifier: http://orcid.org/0000-0002-6177-7062
authors.initials: AC
authors.lastname: Goodeve
authors.affiliation: Haemostasis Research Group, Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, UK. d.hampshire@shef.ac.uk.
authors.forename: D J
authors.identifier: http://orcid.org/0000-0002-1387-8926
authors.initials: DJ
authors.lastname: Hampshire
mesh_terms: D001483:Base Sequence; D056915:DNA Copy Number Variations; D005091:Exons; D006801:Humans; D008969:Molecular Sequence Data; D020641:Polymorphism, Single Nucleotide; D016415:Sequence Alignment; D017384:Sequence Deletion; D014841:von Willebrand Factor / Q000235:genetics*
chemical_list: D014841:von Willebrand Factor