Literature DB >> 10206684

The identification of five novel mutations in the lysosomal acid a-(1-4) glucosidase gene from patients with glycogen storage disease type II. Mutations in brief no. 134. Online.

C E Beesley1, A H Child, M H Yacoub.   

Abstract

The autosomal recessive disorder Glycogen Storage Type II (GSDII) is caused by a deficiency in the lysosomal enzyme acid alpha-glucosidase. We have optimised a procedure to use fluorescent DNA sequencing technology to screen for mutations within the alpha-glucosidase gene from UK patients with GSDII. Five previously unknown mutations in six patients (4 early onset infantile and 2 late adult) have been found. The mutations are an insertion of a C residue in exon 2 (InsC258), an insertion of a G residue in exon 16 (InsG2242), a deletion of 20 nucleotides in exon 4 delta, and a nonsense mutation in exon 16 (G2237A-Trp746Stop). All will result in the introduction of a premature stop codon in the coding region, predicting a truncated and non-functional protein. The final mutation is a duplication of 18 nucleotides in exon 19 (Ins18nt2776) and will result in the insertion of an additional six amino acids into the protein chain after Asn925 (Gly-Val-Pro-Val-Ser-Asn).

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Year:  1998        PMID: 10206684     DOI: 10.1002/(SICI)1098-1004(1998)11:5<413::AID-HUMU16>3.0.CO;2-I

Source DB:  PubMed          Journal:  Hum Mutat        ISSN: 1059-7794            Impact factor:   4.878


  6 in total

1.  Identification and Functional Characterization of GAA Mutations in Colombian Patients Affected by Pompe Disease.

Authors:  Mónica Yasmín Niño; Heidi Eliana Mateus; Dora Janeth Fonseca; Marian A Kroos; Sandra Yaneth Ospina; Juan Fernando Mejía; Jesús Alfredo Uribe; Arnold J J Reuser; Paul Laissue
Journal:  JIMD Rep       Date:  2012-04-19

2.  Predicting cross-reactive immunological material (CRIM) status in Pompe disease using GAA mutations: lessons learned from 10 years of clinical laboratory testing experience.

Authors:  Deeksha S Bali; Jennifer L Goldstein; Suhrad Banugaria; Jian Dai; Joanne Mackey; Catherine Rehder; Priya S Kishnani
Journal:  Am J Med Genet C Semin Med Genet       Date:  2012-01-17       Impact factor: 3.908

3.  Rapidly Progressive White Matter Involvement in Early Childhood: The Expanding Phenotype of Infantile Onset Pompe?

Authors:  A Broomfield; J Fletcher; P Hensman; R Wright; H Prunty; J Pavaine; S A Jones
Journal:  JIMD Rep       Date:  2017-07-20

4.  Variable clinical features and genotype-phenotype correlations in 18 patients with late-onset Pompe disease.

Authors:  Jousef Alandy-Dy; Marie Wencel; Kathy Hall; Julie Simon; Yanjun Chen; Erik Valenti; Jade Yang; Deeksha Bali; Anita Lakatos; Namita Goyal; Tahseen Mozaffar; Virginia Kimonis
Journal:  Ann Transl Med       Date:  2019-07

5.  Clinical Laboratory Experience of Blood CRIM Testing in Infantile Pompe Disease.

Authors:  Deeksha S Bali; Jennifer L Goldstein; Catherine Rehder; Zoheb B Kazi; Kathryn L Berrier; Jian Dai; Priya S Kishnani
Journal:  Mol Genet Metab Rep       Date:  2015-12-01

6.  A nonsense mutation in the acid α-glucosidase gene causes Pompe disease in Finnish and Swedish Lapphunds.

Authors:  Eija H Seppälä; Arnold J J Reuser; Hannes Lohi
Journal:  PLoS One       Date:  2013-02-14       Impact factor: 3.240

  6 in total

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