Editing Wilson's disease (section)

==In other animals==
Hereditary copper accumulation has been described in [[Bedlington Terrier]]s,<ref>{{cite journal  |vauthors=Sternlieb I, Twedt DC, Johnson GF, etal |title=Inherited copper toxicity of the liver in Bedlington terriers |journal=Proc. R. Soc. Med. |volume=70 |issue= Suppl 3|pages=8–9 |year=1977 |doi=10.1177/00359157770700S305 |pmid=122681 |pmc=1543595}}</ref> where it generally only affects the liver. In Bedlington Terriers it is due to mutations in the ''[[COMMD1]]'' (or ''MURR1'') gene.<ref>{{cite journal |vauthors=van De Sluis B, Rothuizen J, Pearson PL, van Oost BA, Wijmenga C |title=Identification of a new copper metabolism gene by positional cloning in a purebred dog population |journal=Hum. Mol. Genet. |volume=11 |issue=2 |pages=165–73 |year=2002 |pmid=11809725 |doi=10.1093/hmg/11.2.165 |doi-access=free }}</ref> The discovery of these mutations in the dogs led researchers to examine the corresponding human genes, but ''COMMD1'' mutations could not be detected in humans with non-Wilsonian copper accumulation states (such as [[Indian childhood cirrhosis]]).<ref>{{cite journal  |vauthors=Müller T, van de Sluis B, Zhernakova A, etal |title=The canine copper toxicosis gene MURR1 does not cause non-Wilsonian hepatic copper toxicosis |journal=J. Hepatol. |volume=38 |issue=2 |pages=164–68 |year=2003 |pmid=12547404 |doi=10.1016/S0168-8278(02)00356-2}}</ref>