{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,8]],"date-time":"2026-06-08T15:27:10Z","timestamp":1780932430634,"version":"3.54.1"},"reference-count":39,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","license":[{"start":{"date-parts":[[2022,3,10]],"date-time":"2022-03-10T00:00:00Z","timestamp":1646870400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Hepatol Commun"],"published-print":{"date-parts":[[2022,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n          <jats:p>Wilson disease (WD) is caused by biallelic pathogenic variants in adenosine triphosphatase copper\u2010transporting beta (ATP7B); however, genetic testing identifies only one or no pathogenic ATP7B variant in a number of patients with WD. Synonymous single\u2010nucleotide sequence variants have been recognized as pathogenic in individual families. The aim of the present study was to evaluate the prevalence and disease mechanism of the synonymous variant c.2292C&gt;T (p.Phe764=) in WD. A cohort of 280 patients with WD heterozygous for a single ATP7B variant was investigated for the presence of c.2292C&gt;T (p.Phe764=). In this cohort of otherwise genetically unexplained WD, the allele frequency of c.2292C&gt;T (p.Phe764=) was 2.5% (14 of 560) compared to 7.1 \u00d7 10<jats:sup>\u22126<\/jats:sup> in the general population (2 of 280,964 in the Genome Aggregation Database; <jats:italic toggle=\"yes\">p<\/jats:italic> &lt; 10<jats:sup>\u22125<\/jats:sup>; Fisher exact test). In an independent United Kingdom (UK) cohort, 2 patients with WD homozygous for p.Phe764= were identified. RNA analysis of ATP7B transcripts from patients homozygous or heterozygous for c.2292C&gt;T and control fibroblasts showed that this variant caused high expression of an ATP7B transcript variant lacking exon 8. Conclusion: The synonymous ATP7B variant c.2292C&gt;T (p.Phe764=) causes abnormal messenger RNA processing of ATP7B transcripts and is associated with WD in compound heterozygotes and homozygotes.<\/jats:p>","DOI":"10.1002\/hep4.1922","type":"journal-article","created":{"date-parts":[[2022,3,10]],"date-time":"2022-03-10T17:26:46Z","timestamp":1646933206000},"page":"1611-1619","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":17,"title":["Synonymous mutation in adenosine triphosphatase copper\u2010transporting beta causes enhanced exon skipping in Wilson disease"],"prefix":"10.1097","volume":"6","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1957-412X","authenticated-orcid":false,"given":"Marlene","family":"Panzer","sequence":"first","affiliation":[{"name":"Department of Medicine I,Medical University of Innsbruck,Innsbruck,Austria"},{"name":"VASCage Research Center on Vascular Ageing and Stroke,Innsbruck,Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7141-8867","authenticated-orcid":false,"given":"Andr\u00e9","family":"Viveiros","sequence":"additional","affiliation":[{"name":"Department of Medicine I,Medical University of Innsbruck,Innsbruck,Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8690-2774","authenticated-orcid":false,"given":"Benedikt","family":"Schaefer","sequence":"additional","affiliation":[{"name":"Department of Medicine I,Medical University of Innsbruck,Innsbruck,Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nadja","family":"Baumgartner","sequence":"additional","affiliation":[{"name":"Department of Medicine I,Medical University of Innsbruck,Innsbruck,Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6503-1455","authenticated-orcid":false,"given":"Klaus","family":"Seppi","sequence":"additional","affiliation":[{"name":"Department of Neurology,Medical University of Innsbruck,Innsbruck,Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7174-6000","authenticated-orcid":false,"given":"Atbin","family":"Djamshidian","sequence":"additional","affiliation":[{"name":"Department of Neurology,Medical University of Innsbruck,Innsbruck,Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0548-5487","authenticated-orcid":false,"given":"Theodor","family":"Todorov","sequence":"additional","affiliation":[{"name":"Department of Medical Genetics and Molecular Biology,University Hospital Lozenetz,Sofia,Bulgaria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9927-0868","authenticated-orcid":false,"given":"William J. 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