Associations between multiple system atrophy and polymorphisms of SLC1A4, SQSTM1, and EIF4EBP1 Genes
Identifieur interne : 002987 ( Main/Exploration ); précédent : 002986; suivant : 002988Associations between multiple system atrophy and polymorphisms of SLC1A4, SQSTM1, and EIF4EBP1 Genes
Auteurs : Hiroyuki Soma [Japon] ; Ichiro Yabe [Japon] ; Asako Takei [Japon] ; Naoto Fujiki [Japon] ; Tetsuro Yanagihara [Japon] ; Hidenao Sasaki [Japon]Source :
- Movement Disorders [ 0885-3185 ] ; 2008-06-15.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Adaptor Proteins, Signal Transducing (genetics), Adult, Aged, Alleles, Binding protein, Carrier, Excitatory Amino Acid Transporter 3 (genetics), Female, Gene Frequency (genetics), Genotype, Haplotypes, Humans, Initiation factor, Linkage Disequilibrium (genetics), Male, Middle Aged, Multiple System Atrophy (genetics), Multiple system atrophy, Nervous system diseases, Oxidative Stress (genetics), Oxidative stress, Phosphoproteins (genetics), Polymorphism, Single Nucleotide (genetics), Single nucleotide polymorphism, eukaryotic translation initiation factor 4E‐binding protein 1, multiple system atrophy, oxidative stress, sequestosome 1, single‐nucleotide polymorphism, solute carrier family 1A4.
- MESH :
- chemical , genetics : Adaptor Proteins, Signal Transducing, Excitatory Amino Acid Transporter 3, Phosphoproteins.
- genetics : Gene Frequency, Linkage Disequilibrium, Multiple System Atrophy, Oxidative Stress, Polymorphism, Single Nucleotide.
- Adult, Aged, Alleles, Female, Genotype, Haplotypes, Humans, Male, Middle Aged.
Abstract
Multiple system atrophy (MSA) is an adult‐onset sporadic neurodegenerative disease. Although the etiology of MSA remains obscure, recent studies suggest that oxidative stress is associated with the pathogenesis of MSA. The aim of this study was to evaluate genetic associations between the candidate genes involved in oxidative stress and MSA in a case‐control study. We examined 119 Japanese patients with MSA and 123 controls, and genotyped single‐nucleotide polymorphisms (SNPs) of the following eight genes: CCAAT/enhancer‐binding protein homologous protein, activating transcription factor 3, CCAAT/enhancer‐binding protein‐β, sequestosome 1 (SQSTM1), cysteinyl‐tRNA synthetase, solute carrier family 1A4 (SLC1A4), activating transcription factor 4, and eukaryotic translation initiation factor 4E‐binding protein 1 (EIF4EBP1). SLC1A4 SNP +28833 (V398I, rs759458, genotype: Pc = 0.0186, allele: Pc = 0.0303, Pc: P‐value with Bonferroni correction), two major haplotypes of SLC1A4 “T‐C‐C‐G” and “T‐C‐T‐A” (Pc = 0.0261 and 0.000768), two‐SNP haplotypes of SQSTM1 “C‐T” and “A‐T” (Pc = 0.0136 and 0.0369), and the most common haplotype of EIF4EBP1 “C‐T‐G‐C” (Pc = 0.0480) showed significant associations. This study revealed genetic associations of SLC1A4, SQSTM1, and EIF4EBP1 with MSA. These results may lend genetic support to the hypothesis that oxidative stress is associated with the pathogenesis of MSA. © 2008 Movement Disorder Society
Url:
DOI: 10.1002/mds.22046
Affiliations:
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uniqKey="Fujiki N" first="Naoto" last="Fujiki">Naoto Fujiki</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neurology, Sapporo Minami National Hospital, Sapporo, Hokkaido</wicri:regionArea><wicri:noRegion>Hokkaido</wicri:noRegion></affiliation></author><author><name sortKey="Yanagihara, Tetsuro" sort="Yanagihara, Tetsuro" uniqKey="Yanagihara T" first="Tetsuro" last="Yanagihara">Tetsuro Yanagihara</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Ebetsu Neurology Clinic, Ebetsu, Hokkaido</wicri:regionArea><wicri:noRegion>Hokkaido</wicri:noRegion></affiliation></author><author><name sortKey="Sasaki, Hidenao" sort="Sasaki, Hidenao" uniqKey="Sasaki H" first="Hidenao" last="Sasaki">Hidenao Sasaki</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neurology, Hokkaido University Graduate School of Medicine, Sapporo, 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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2008-06-15">2008-06-15</date><biblScope unit="vol">23</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="1161">1161</biblScope><biblScope unit="page" to="1167">1167</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">DE1FE038223518B4DB5553073894F888383CAA69</idno><idno type="DOI">10.1002/mds.22046</idno><idno type="ArticleID">MDS22046</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptor Proteins, Signal Transducing (genetics)</term><term>Adult</term><term>Aged</term><term>Alleles</term><term>Binding protein</term><term>Carrier</term><term>Excitatory Amino Acid Transporter 3 (genetics)</term><term>Female</term><term>Gene Frequency (genetics)</term><term>Genotype</term><term>Haplotypes</term><term>Humans</term><term>Initiation factor</term><term>Linkage Disequilibrium (genetics)</term><term>Male</term><term>Middle Aged</term><term>Multiple System Atrophy (genetics)</term><term>Multiple system atrophy</term><term>Nervous system diseases</term><term>Oxidative Stress (genetics)</term><term>Oxidative stress</term><term>Phosphoproteins (genetics)</term><term>Polymorphism, Single Nucleotide (genetics)</term><term>Single nucleotide polymorphism</term><term>eukaryotic translation initiation factor 4E‐binding protein 1</term><term>multiple system atrophy</term><term>oxidative stress</term><term>sequestosome 1</term><term>single‐nucleotide polymorphism</term><term>solute carrier family 1A4</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term><term>Excitatory Amino Acid Transporter 3</term><term>Phosphoproteins</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Gene Frequency</term><term>Linkage Disequilibrium</term><term>Multiple System Atrophy</term><term>Oxidative Stress</term><term>Polymorphism, Single Nucleotide</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Alleles</term><term>Female</term><term>Genotype</term><term>Haplotypes</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Atrophie multisystématisée</term><term>Facteur initiation</term><term>Pathologie du système nerveux</term><term>Polymorphisme mononucléotide</term><term>Porteur</term><term>Protéine liaison</term><term>Stress oxydatif</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Multiple system atrophy (MSA) is an adult‐onset sporadic neurodegenerative disease. Although the etiology of MSA remains obscure, recent studies suggest that oxidative stress is associated with the pathogenesis of MSA. The aim of this study was to evaluate genetic associations between the candidate genes involved in oxidative stress and MSA in a case‐control study. We examined 119 Japanese patients with MSA and 123 controls, and genotyped single‐nucleotide polymorphisms (SNPs) of the following eight genes: CCAAT/enhancer‐binding protein homologous protein, activating transcription factor 3, CCAAT/enhancer‐binding protein‐β, sequestosome 1 (SQSTM1), cysteinyl‐tRNA synthetase, solute carrier family 1A4 (SLC1A4), activating transcription factor 4, and eukaryotic translation initiation factor 4E‐binding protein 1 (EIF4EBP1). SLC1A4 SNP +28833 (V398I, rs759458, genotype: Pc = 0.0186, allele: Pc = 0.0303, Pc: P‐value with Bonferroni correction), two major haplotypes of SLC1A4 “T‐C‐C‐G” and “T‐C‐T‐A” (Pc = 0.0261 and 0.000768), two‐SNP haplotypes of SQSTM1 “C‐T” and “A‐T” (Pc = 0.0136 and 0.0369), and the most common haplotype of EIF4EBP1 “C‐T‐G‐C” (Pc = 0.0480) showed significant associations. This study revealed genetic associations of SLC1A4, SQSTM1, and EIF4EBP1 with MSA. These results may lend genetic support to the hypothesis that oxidative stress is associated with the pathogenesis of MSA. © 2008 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Japon</li></country></list><tree><country name="Japon"><noRegion><name sortKey="Soma, Hiroyuki" sort="Soma, Hiroyuki" uniqKey="Soma H" first="Hiroyuki" last="Soma">Hiroyuki Soma</name></noRegion><name sortKey="Fujiki, Naoto" sort="Fujiki, Naoto" uniqKey="Fujiki N" first="Naoto" last="Fujiki">Naoto Fujiki</name><name sortKey="Sasaki, Hidenao" sort="Sasaki, Hidenao" uniqKey="Sasaki H" first="Hidenao" last="Sasaki">Hidenao Sasaki</name><name sortKey="Takei, Asako" sort="Takei, Asako" uniqKey="Takei A" first="Asako" last="Takei">Asako Takei</name><name sortKey="Yabe, Ichiro" sort="Yabe, Ichiro" uniqKey="Yabe I" first="Ichiro" last="Yabe">Ichiro Yabe</name><name sortKey="Yanagihara, Tetsuro" sort="Yanagihara, Tetsuro" uniqKey="Yanagihara T" first="Tetsuro" last="Yanagihara">Tetsuro Yanagihara</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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