Literature DB >> 17361008

Genomic deletion within GLDC is a major cause of non-ketotic hyperglycinaemia.

Junko Kanno, Tim Hutchin, Fumiaki Kamada, Ayumi Narisawa, Yoko Aoki, Yoichi Matsubara, Shigeo Kure.   

Abstract

BACKGROUND: Non-ketotic hyperglycinaemia (NKH) is an inborn error of metabolism characterised by accumulation of glycine in body fluids and various neurological symptoms. NKH is caused by deficiency of the glycine cleavage multienzyme system with three specific components encoded by GLDC, AMT and GCSH. Most patients are deficient of the enzymatic activity of glycine decarboxylase, which is encoded by GLDC. Our recent study has suggested that there are a considerable number of GLDC mutations which are not identified by the standard exon-sequencing method.
METHODS: A screening system for GLDC deletions by multiplex ligation-dependent probe amplification (MLPA) has been developed. Two distinct cohorts of patients with typical NKH were screened by this
METHOD: the first cohort consisted of 45 families with no identified AMT or GCSH mutations, and the second cohort was comprised of 20 patients from the UK who were not prescreened for AMT mutations.
RESULTS: GLDC deletions were identified in 16 of 90 alleles (18%) in the first cohort and in 9 of 40 alleles (22.5%) in the second cohort. 14 different types of deletions of various lengths were identified, including one allele where all 25 exons were missing. Flanking sequences of interstitial deletions in five patients were determined, and Alu-mediated recombination was identified in three of five patients.
CONCLUSIONS: GLDC deletions are a significant cause of NKH, and the MLPA analysis is a valuable first-line screening for NKH genetic testing.

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Year:  2007        PMID: 17361008      PMCID: PMC2598024          DOI: 10.1136/jmg.2006.043448

Source DB:  PubMed          Journal:  J Med Genet        ISSN: 0022-2593            Impact factor:   6.318


  28 in total

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3.  Mild variant of nonketotic hyperglycinemia with typical neonatal presentations: mutational and in vitro expression analyses in two patients.

Authors:  Shigeo Kure; Akiko Ichinohe; Kanako Kojima; Kenichi Sato; Zenro Kizaki; Fumio Inoue; Chutaro Yamanaka; Yoichi Matsubara
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6.  Human glycine decarboxylase gene (GLDC) and its highly conserved processed pseudogene (psiGLDC): their structure and expression, and the identification of a large deletion in a family with nonketotic hyperglycinemia.

Authors:  M Takayanagi; S Kure; Y Sakata; Y Kurihara; Y Ohya; M Kajita; K Tada; Y Matsubara; K Narisawa
Journal:  Hum Genet       Date:  2000-03       Impact factor: 4.132

7.  Chromosomal localization, structure, single-nucleotide polymorphisms, and expression of the human H-protein gene of the glycine cleavage system (GCSH), a candidate gene for nonketotic hyperglycinemia.

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9.  Comprehensive mutation analysis of GLDC, AMT, and GCSH in nonketotic hyperglycinemia.

Authors:  Shigeo Kure; Kumi Kato; Agirios Dinopoulos; Chuck Gail; Ton J DeGrauw; John Christodoulou; Vladimir Bzduch; Rozalia Kalmanchey; Gyorgy Fekete; Alex Trojovsky; Barbara Plecko; Galen Breningstall; Jun Tohyama; Yoko Aoki; Yoichi Matsubara
Journal:  Hum Mutat       Date:  2006-04       Impact factor: 4.878

10.  Two-color multiplex ligation-dependent probe amplification: detecting genomic rearrangements in hereditary multiple exostoses.

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4.  R-loopDB: a database for R-loop forming sequences (RLFS) and R-loops.

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5.  Mutation analysis of glycine decarboxylase, aminomethyltransferase and glycine cleavage system protein-H genes in 13 unrelated families with glycine encephalopathy.

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Journal:  Clin Pharmacol Ther       Date:  2010-11-24       Impact factor: 6.875

7.  [Clinical and molecular genetic study of nonketotic hyperglycinemia in a Chinese family].

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9.  The genetic basis of classic nonketotic hyperglycinemia due to mutations in GLDC and AMT.

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10.  Genotypic and phenotypic features in Turkish patients with classic nonketotic hyperglycinemia.

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