A 5' splice junction mutation leading to exon deletion in an Ashkenazic Jewish family with phosphofructokinase deficiency (Tarui disease).
Open Access
- 1 March 1993
- journal article
- case report
- Published by Elsevier in Journal of Biological Chemistry
- Vol. 268 (7) , 4963-4967
- https://doi.org/10.1016/s0021-9258(18)53489-x
Abstract
No abstract availableKeywords
This publication has 39 references indexed in Scilit:
- Cloning and Characterization of the Human Muscle Phosphofructokinase GeneDNA and Cell Biology, 1992
- Three novel mutations in the cystic fibrosis gene detected by chemical cleavage: analysis of variant splicing and a nonsense mutationHuman Molecular Genetics, 1992
- Effect of dystrophin gene deletions on mRNA levels and processing in Duchenne and Becker muscular dystrophiesCell, 1990
- Evidence for alternative RNA splicing and possible alternative promoters in the human muscle phosphofructokinase gene at the 5′ untranslated regionBiochemical and Biophysical Research Communications, 1989
- Identification of an altered splice site in Ashkenazi Tay-Sachs diseaseNature, 1988
- A splicing defect due to an exon-intron junctional mutation results in abnormal β-hexosaminidase α chain mRNAs in Ashkenazi Jewish patients with Tay-Sachs diseaseBiochemical and Biophysical Research Communications, 1988
- Cloning of human muscle phosphofructokinase cDNAFEBS Letters, 1987
- Sequence requirements for splicing of higher eukaryotic nuclear pre-mRNACell, 1986
- Heterogeneity of the molecular lesions in inherited phosphofructokinase deficiency.Journal of Clinical Investigation, 1983
- Phosphofructokinase deficiency in skeletal muscle. A new type of glycogenosisBiochemical and Biophysical Research Communications, 1965