Novel mutation in the TOR1A (DYT1) gene in atypical early onset dystonia and polymorphisms in dystonia and early onset parkinsonism.
Identifieur interne : 000246 ( PubMed/Corpus ); précédent : 000245; suivant : 000247Novel mutation in the TOR1A (DYT1) gene in atypical early onset dystonia and polymorphisms in dystonia and early onset parkinsonism.
Auteurs : J Leung ; C. Klein ; J. Friedman ; P. Vieregge ; H. Jacobs ; D. Doheny ; C. Kamm ; D. Deleon ; P Pramstaller ; J Penney ; M. Eisengart ; J. Jankovic ; T. Gasser ; S Bressman ; D Corey ; P. Kramer ; M Brin ; L Ozelius ; X BreakefieldSource :
- Neurogenetics [ 1364-6745 ] ; 2001.
English descriptors
- KwdEn :
- Adolescent, Adult, Age of Onset, Carrier Proteins (genetics), Child, Child, Preschool, DNA Primers, Dystonia Musculorum Deformans (genetics), Female, Humans, Infant, Male, Middle Aged, Molecular Chaperones, Mutation, Parkinson Disease (genetics), Pedigree, Polymerase Chain Reaction, Polymorphism, Genetic, Polymorphism, Single-Stranded Conformational, Sequence Deletion.
- MESH :
- chemical , genetics : Carrier Proteins.
- genetics : Dystonia Musculorum Deformans, Parkinson Disease.
- Adolescent, Adult, Age of Onset, Child, Child, Preschool, DNA Primers, Female, Humans, Infant, Male, Middle Aged, Molecular Chaperones, Mutation, Pedigree, Polymerase Chain Reaction, Polymorphism, Genetic, Polymorphism, Single-Stranded Conformational, Sequence Deletion.
Abstract
Dystonia is a movement disorder involving sustained muscle contractions and abnormal posturing with a strong hereditary predisposition and without a distinct neuropathology. In this study the TOR1A (DYT1) gene was screened for mutations in cases of early onset dystonia and early onset parkinsonism (EOP), which frequently presents with dystonic symptoms. In a screen of 40 patients, we identified three variations, none of which occurred in EOP patients. Two infrequent intronic single base pair (bp) changes of unknown consequences were found in a dystonia patient and the mother of an EOP patient. An 18-bp deletion (Phe323_Tyr328del) in the TOR1A gene was found in a patient with early onset dystonia and myoclonic features. This deletion would remove 6 amino acids close to the carboxy terminus, including a putative phosphorylation site of torsinA. This 18-bp deletion is the first additional mutation, beyond the GAG-deletion (Glu302/303del), to be found in the TOR1A gene, and is associated with a distinct type of early onset dystonia.
PubMed: 11523564
Links to Exploration step
pubmed:11523564Le document en format XML
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<term>Child</term>
<term>Child, Preschool</term>
<term>DNA Primers</term>
<term>Dystonia Musculorum Deformans (genetics)</term>
<term>Female</term>
<term>Humans</term>
<term>Infant</term>
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<term>Mutation</term>
<term>Parkinson Disease (genetics)</term>
<term>Pedigree</term>
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<front><div type="abstract" xml:lang="en">Dystonia is a movement disorder involving sustained muscle contractions and abnormal posturing with a strong hereditary predisposition and without a distinct neuropathology. In this study the TOR1A (DYT1) gene was screened for mutations in cases of early onset dystonia and early onset parkinsonism (EOP), which frequently presents with dystonic symptoms. In a screen of 40 patients, we identified three variations, none of which occurred in EOP patients. Two infrequent intronic single base pair (bp) changes of unknown consequences were found in a dystonia patient and the mother of an EOP patient. An 18-bp deletion (Phe323_Tyr328del) in the TOR1A gene was found in a patient with early onset dystonia and myoclonic features. This deletion would remove 6 amino acids close to the carboxy terminus, including a putative phosphorylation site of torsinA. This 18-bp deletion is the first additional mutation, beyond the GAG-deletion (Glu302/303del), to be found in the TOR1A gene, and is associated with a distinct type of early onset dystonia.</div>
</front>
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<Abstract><AbstractText>Dystonia is a movement disorder involving sustained muscle contractions and abnormal posturing with a strong hereditary predisposition and without a distinct neuropathology. In this study the TOR1A (DYT1) gene was screened for mutations in cases of early onset dystonia and early onset parkinsonism (EOP), which frequently presents with dystonic symptoms. In a screen of 40 patients, we identified three variations, none of which occurred in EOP patients. Two infrequent intronic single base pair (bp) changes of unknown consequences were found in a dystonia patient and the mother of an EOP patient. An 18-bp deletion (Phe323_Tyr328del) in the TOR1A gene was found in a patient with early onset dystonia and myoclonic features. This deletion would remove 6 amino acids close to the carboxy terminus, including a putative phosphorylation site of torsinA. This 18-bp deletion is the first additional mutation, beyond the GAG-deletion (Glu302/303del), to be found in the TOR1A gene, and is associated with a distinct type of early onset dystonia.</AbstractText>
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