Impaired glycosylation and cutis laxa caused by mutations in the vesicular H+-ATPase subunit ATP6V0A2.
Journal: Nature Genetics
Published:
Abstract
We identified loss-of-function mutations in ATP6V0A2, encoding the a2 subunit of the V-type H+ ATPase, in several families with autosomal recessive cutis laxa type II or wrinkly skin syndrome. The mutations result in abnormal glycosylation of serum proteins (CDG-II) and cause an impairment of Golgi trafficking in fibroblasts from affected individuals. These results indicate that the a2 subunit of the proton pump has an important role in Golgi function.
Authors
Uwe Kornak, Ellen Reynders, Aikaterini Dimopoulou, Jeroen Van Reeuwijk, Bjoern Fischer, Anna Rajab, Birgit Budde, Peter Nürnberg, Francois Foulquier, Zsolt Urban, Stephanie Gruenewald, Wim Annaert, Han Brunner, Hans Van Bokhoven, Ron Wevers, Eva Morava, Gert Matthijs, Lionel Van Maldergem, Stefan Mundlos
Relevant Conditions