| Literature DB >> 17047887 |
Yoriko Endo1, Asako Horinishi1, Matthias Vorgerd2, Yoshiko Aoyama1, Tetsu Ebara1, Toshio Murase1, Masato Odawara3, Teodor Podskarbi4, Yoon S Shin5, Minoru Okubo6,7.
Abstract
Glycogen storage disease type III (GSD III) is an autosomal recessive disorder characterized by excessive accumulation of abnormal glycogen in the liver and/or muscles and caused by deficiency in the glycogen debranching enzyme (AGL). Previous studies have revealed that the spectrum of AGL mutations in GSD III patients depends on ethnic grouping. We investigated nine GSD III patients from Germany, Canada, Afghanistan, Iran, and Turkey and identified six novel AGL mutations: one nonsense (W255X), three deletions (1019delA, 3202-3203delTA, and 1859-1869del11-bp), and two splicing mutations (IVS7 + 5G > A and IVS21 + 5insA), together with three previously reported ones (R864X, W1327X, and IVS21 + 1G > A). All mutations are predicted to lead to premature termination, which abolishes enzyme activity. Our molecular study on GSD III patients of different ethnic ancestry showed allelic heterogeneity of AGL mutations. This is the first AGL mutation report for German, Canadian, Afghan, Iranian and Turkish populations.Entities:
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Year: 2006 PMID: 17047887 DOI: 10.1007/s10038-006-0045-x
Source DB: PubMed Journal: J Hum Genet ISSN: 1434-5161 Impact factor: 3.172