MovDisordV3, PascalFrancis, Curation, bibRecord, 000952

Developments in the molecular biology of DYT1 dystonia

Identifieur interne : 000952 ( PascalFrancis/Curation ); précédent : 000951; suivant : 000953

Developments in the molecular biology of DYT1 dystonia

Auteurs : Ruth H. Walker [États-Unis] ; P. Shashidharan [États-Unis]

Source :

Movement disorders [ 0885-3185 ] ; 2003.

RBID : Pascal:04-0095344

Descripteurs français

Pascal (Inist)
- Dystonie, Mutation, Immunohistochimie, Pénétrance génique, Biologie moléculaire, Déterminisme génétique, Homme, Souris, Animal transgénique, Gène DYT1, TorsinA.
Wicri :
- topic : Homme, Animal transgénique.

English descriptors

KwdEn :
- Dystonia, Gene penetrance, Genetic determinism, Human, Immunohistochemistry, Molecular biology, Mouse, Mutation, Transgenic animal.

Abstract

The identification of a mutation of the DYTI gene as a cause of inherited dystonia has led to many insights regarding the genetics of this disorder. In addition, there is a rapidly expanding list of inherited dystonia syndromes, the genes for some of which have been identified or localized. The DYTI mutation has been found in a variety of ethnic groups, and it may result in a range of phenotypes. To date, studies of torsinA, the protein product of the DYTI gene, have not revealed its function, although its widespread distribution throughout the central nervous system suggests a universal role. TorsinA has structural homology to heat shock and chaperone proteins. Evidence from studies in cell cultures and Caenorhabditis elegans, and the presence of torsinA in inclusion bodies in several neurodegenerative diseases may be indicative of function of this nature. Preliminary studies in humans with DYTI dystonia and in DYTI transgenic mice suggest disruption of the dopaminergic nigrostriatal system. A functional interference with neuronal signal processing induced by mutation of torsinA is consistent with current hypotheses regarding impairment of the center-surround mechanism in the striatum.

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C01	`01`		`ENG`	@0 The identification of a mutation of the DYTI gene as a cause of inherited dystonia has led to many insights regarding the genetics of this disorder. In addition, there is a rapidly expanding list of inherited dystonia syndromes, the genes for some of which have been identified or localized. The DYTI mutation has been found in a variety of ethnic groups, and it may result in a range of phenotypes. To date, studies of torsinA, the protein product of the DYTI gene, have not revealed its function, although its widespread distribution throughout the central nervous system suggests a universal role. TorsinA has structural homology to heat shock and chaperone proteins. Evidence from studies in cell cultures and Caenorhabditis elegans, and the presence of torsinA in inclusion bodies in several neurodegenerative diseases may be indicative of function of this nature. Preliminary studies in humans with DYTI dystonia and in DYTI transgenic mice suggest disruption of the dopaminergic nigrostriatal system. A functional interference with neuronal signal processing induced by mutation of torsinA is consistent with current hypotheses regarding impairment of the center-surround mechanism in the striatum.
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C03	`06`	`X`	`FRE`	`@0 Déterminisme génétique @5 18`
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C03	`09`	`X`	`ENG`	`@0 Transgenic animal @5 22`
C03	`09`	`X`	`SPA`	`@0 Animal transgénico @5 22`
C03	`10`	`X`	`FRE`	`@0 Gène DYT1 @4 INC @5 86`
C03	`11`	`X`	`FRE`	`@0 TorsinA @4 INC @5 87`
C07	`01`	`X`	`FRE`	`@0 Rodentia @2 NS`
C07	`01`	`X`	`ENG`	`@0 Rodentia @2 NS`
C07	`01`	`X`	`SPA`	`@0 Rodentia @2 NS`
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C07	`05`	`X`	`ENG`	`@0 Nervous system diseases @5 38`
C07	`05`	`X`	`SPA`	`@0 Sistema nervioso patología @5 38`
C07	`06`	`X`	`FRE`	`@0 Trouble neurologique @5 39`
C07	`06`	`X`	`ENG`	`@0 Neurological disorder @5 39`
C07	`06`	`X`	`SPA`	`@0 Trastorno neurológico @5 39`
C07	`07`	`X`	`FRE`	`@0 Mouvement involontaire @5 40`
C07	`07`	`X`	`ENG`	`@0 Involuntary movement @5 40`
C07	`07`	`X`	`SPA`	`@0 Movimiento involuntario @5 40`
C07	`08`	`X`	`FRE`	`@0 Extrapyramidal syndrome @5 41`
C07	`08`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 41`
C07	`08`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 41`
C07	`09`	`X`	`FRE`	`@0 Maladie héréditaire @5 42`
C07	`09`	`X`	`ENG`	`@0 Genetic disease @5 42`
C07	`09`	`X`	`SPA`	`@0 Enfermedad hereditaria @5 42`
C07	`10`	`X`	`FRE`	`@0 Anatomopathologie @5 53`
C07	`10`	`X`	`ENG`	`@0 Anatomic pathology @5 53`
C07	`10`	`X`	`SPA`	`@0 Anatomía patológica @5 53`
N21				`@1 061`
N82				`@1 PSI`

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Le document en format XML

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<front><div type="abstract" xml:lang="en">The identification of a mutation of the DYTI gene as a cause of inherited dystonia has led to many insights regarding the genetics of this disorder. In addition, there is a rapidly expanding list of inherited dystonia syndromes, the genes for some of which have been identified or localized. The DYTI mutation has been found in a variety of ethnic groups, and it may result in a range of phenotypes. To date, studies of torsinA, the protein product of the DYTI gene, have not revealed its function, although its widespread distribution throughout the central nervous system suggests a universal role. TorsinA has structural homology to heat shock and chaperone proteins. Evidence from studies in cell cultures and Caenorhabditis elegans, and the presence of torsinA in inclusion bodies in several neurodegenerative diseases may be indicative of function of this nature. Preliminary studies in humans with DYTI dystonia and in DYTI transgenic mice suggest disruption of the dopaminergic nigrostriatal system. A functional interference with neuronal signal processing induced by mutation of torsinA is consistent with current hypotheses regarding impairment of the center-surround mechanism in the striatum.</div>
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<s5>07</s5>
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<s5>10</s5>
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<s5>10</s5>
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<s5>18</s5>
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<s5>21</s5>
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<s5>21</s5>
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<s5>21</s5>
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<s4>INC</s4>
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<s4>INC</s4>
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<s2>NS</s2>
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<fC07 i1="01" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
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<fC07 i1="01" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
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<s2>NS</s2>
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<fC07 i1="02" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
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<fC07 i1="03" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
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<fC07 i1="03" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
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<fC07 i1="03" i2="X" l="SPA"><s0>Vertebrata</s0>
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<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Trouble neurologique</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Neurological disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Trastorno neurológico</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Mouvement involontaire</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Involuntary movement</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Movimiento involuntario</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Maladie héréditaire</s0>
<s5>42</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Genetic disease</s0>
<s5>42</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Enfermedad hereditaria</s0>
<s5>42</s5>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Anatomopathologie</s0>
<s5>53</s5>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Anatomic pathology</s0>
<s5>53</s5>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Anatomía patológica</s0>
<s5>53</s5>
</fC07>
<fN21><s1>061</s1>
</fN21>
<fN82><s1>PSI</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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	Movement Disorders (revue)
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Movement Disorders (revue)

Developments in the molecular biology of DYT1 dystonia

Developments in the molecular biology of DYT1 dystonia

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