| Literature DB >> 17056254 |
Rachel E Palmer1, Hernan M Amartino, Gabriela Niizawa, Mariana Blanco, Robert J Pomponio, Nestor A Chamoles.
Abstract
Pompe disease is an autosomal recessive disorder caused by a deficiency in 1,4-alpha-glucosidase (EC.3.2.1.3), the enzyme required to hydrolyze lysosomal glycogen to glucose. While previous studies have focused on Pompe patients from Europe, the United States, and Taiwan, we have analyzed a group of South American Pompe patients to better understand the molecular basis of their disease. From 14 Argentinean patients diagnosed with either infantile or late-onset disease, we identified 14 distinct mutations in the acid alpha-glucosidase (GAA) gene including nine novel variants (c.236_246del, c.377G>A, c.1099T>C, c.1397T>G, c.1755-1G>A, c.1802C>G, c.1978C>T, c.2281delGinsAT, and c.2608C>T). Three different families displayed the c.377G>A allelic variant, suggesting a higher frequency among a subset of Argentineans. Comparison of patients with similar or identical variations in the GAA gene highlights the phenotypic diversity of late-onset disease and supports a role for other genetic and environmental factors in disease presentation.Entities:
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Year: 2006 PMID: 17056254 DOI: 10.1016/j.nmd.2006.09.004
Source DB: PubMed Journal: Neuromuscul Disord ISSN: 0960-8966 Impact factor: 4.296