Skip to main content
American Journal of Human Genetics logoLink to American Journal of Human Genetics
. 2016 Aug 2;99(2):521. doi: 10.1016/j.ajhg.2016.07.015

Syndrome of Hepatic Cirrhosis, Dystonia, Polycythemia, and Hypermanganesemia Caused by Mutations in SLC30A10, a Manganese Transporter in Man

Karin Tuschl , Peter T Clayton, Sidney M Gospe Jr, Shamshad Gulab, Shahnaz Ibrahim, Pratibha Singhi, Roosy Aulakh, Reinaldo T Ribeiro, Orlando G Barsottini, Maha S Zaki, Maria Luz Del Rosario, Sarah Dyack, Victoria Price, Andrea Rideout, Kevin Gordon, Ron A Wevers, WK ‘‘Kling’’ Chong, Philippa B Mills
PMCID: PMC4974105  PMID: 27486784

(The American Journal of Human Genetics 90, 457–466; March 9, 2012)

In this article, Figure 1 contained an error regarding the position of the deletion detected in the affected individuals of family A. The no-call SNPs between the coordinates 218,057,426 and 218,158,564 (GRCh36) suggest that exons 3 and 4 of SLC30A10 are deleted, whereas the original figure showed that exons 1 and 2 were deleted. The corrected Figure 1 and its legend are shown here. The authors regret the error.

Figure 1.

Figure 1

SLC30A10 Mutations in Affected Families with a Syndrome of Hepatic Cirrhosis, Dystonia, Polycythemia, and Hypermanganesemia

(A) Mutations in SLC30A10 identified by DNA sequencing. (For families D and G no DNA was available for analysis of deceased siblings D-II-3 and G-II-1.)

(B) Genomic structure of the exons encoding SLC30A10 and positions of identified mutations. The large deletion spanning exons 3 and 4 in family A is indicated by a bracket.


Articles from American Journal of Human Genetics are provided here courtesy of American Society of Human Genetics

RESOURCES