Mitochondrial complex I and IV activities in leukocytes from patients with parkin mutations
Identifieur interne : 001577 ( Istex/Corpus ); précédent : 001576; suivant : 001578Mitochondrial complex I and IV activities in leukocytes from patients with parkin mutations
Auteurs : Meltem Müftüoglu ; Bülent Elibol ; Özlem Dalm Zrak ; Ayse Ercan ; Gülnihal Kulaks Z ; Hamdi Ögüs ; Turgay Dalkara ; Nazmi ÖzerSource :
- Movement Disorders [ 0885-3185 ] ; 2004-05.
English descriptors
- KwdEn :
Abstract
The parkin protein functions as a RING‐type ubiquitin protein ligase. Considering the possibility that impaired ubiquitin‐proteosomal system activity may impair antioxidant defenses and enhance oxidative stress, we have investigated the activity of mitochondrial respiratory enzymes in patients with parkin gene mutations. A significant decrease in the leukocyte complex I activity was found both in patients with parkin mutations (62.5%) and idiopathic PD (64.5%) compared with age‐matched controls (P < 0.001). Complex IV activity was also decreased significantly in idiopathic PD patients (60%), but no difference was detected between controls and patients with parkin mutations. © 2003 Movement Disorder Society
Url:
DOI: 10.1002/mds.10695
Links to Exploration step
ISTEX:FCC69B357943B6FD8B6B059446C76F8D185770F4Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Mitochondrial complex I and IV activities in leukocytes from patients with parkin mutations</title><author><name sortKey="Muftuoglu, Meltem" sort="Muftuoglu, Meltem" uniqKey="Muftuoglu M" first="Meltem" last="Müftüoglu">Meltem Müftüoglu</name><affiliation><mods:affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</mods:affiliation></affiliation></author><author><name sortKey="Elibol, Bulent" sort="Elibol, Bulent" uniqKey="Elibol B" first="Bülent" last="Elibol">Bülent Elibol</name><affiliation><mods:affiliation>Department of Neurology, Hacettepe University, Faculty of Medicine, Ankara, Turkey</mods:affiliation></affiliation></author><author><name sortKey="Dalm Zrak, Ozlem" sort="Dalm Zrak, Ozlem" uniqKey="Dalm Zrak O" first="Özlem" last="Dalm Zrak">Özlem Dalm Zrak</name><affiliation><mods:affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</mods:affiliation></affiliation></author><author><name sortKey="Ercan, Ayse" sort="Ercan, Ayse" uniqKey="Ercan A" first="Ayse" last="Ercan">Ayse Ercan</name><affiliation><mods:affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</mods:affiliation></affiliation></author><author><name sortKey="Kulaks Z, Gulnihal" sort="Kulaks Z, Gulnihal" uniqKey="Kulaks Z G" first="Gülnihal" last="Kulaks Z">Gülnihal Kulaks Z</name><affiliation><mods:affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</mods:affiliation></affiliation></author><author><name sortKey="Ogus, Hamdi" sort="Ogus, Hamdi" uniqKey="Ogus H" first="Hamdi" last="Ögüs">Hamdi Ögüs</name><affiliation><mods:affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</mods:affiliation></affiliation></author><author><name sortKey="Dalkara, Turgay" sort="Dalkara, Turgay" uniqKey="Dalkara T" first="Turgay" last="Dalkara">Turgay Dalkara</name><affiliation><mods:affiliation>Department of Neurology, Hacettepe University, Faculty of Medicine, Ankara, Turkey</mods:affiliation></affiliation></author><author><name sortKey="Ozer, Nazmi" sort="Ozer, Nazmi" uniqKey="Ozer N" first="Nazmi" last="Özer">Nazmi Özer</name><affiliation><mods:affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:FCC69B357943B6FD8B6B059446C76F8D185770F4</idno><date when="2004" year="2004">2004</date><idno type="doi">10.1002/mds.10695</idno><idno type="url">https://api.istex.fr/document/FCC69B357943B6FD8B6B059446C76F8D185770F4/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001577</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Mitochondrial complex I and IV activities in leukocytes from patients with parkin mutations</title><author><name sortKey="Muftuoglu, Meltem" sort="Muftuoglu, Meltem" uniqKey="Muftuoglu M" first="Meltem" last="Müftüoglu">Meltem Müftüoglu</name><affiliation><mods:affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</mods:affiliation></affiliation></author><author><name sortKey="Elibol, Bulent" sort="Elibol, Bulent" uniqKey="Elibol B" first="Bülent" last="Elibol">Bülent Elibol</name><affiliation><mods:affiliation>Department of Neurology, Hacettepe University, Faculty of Medicine, Ankara, Turkey</mods:affiliation></affiliation></author><author><name sortKey="Dalm Zrak, Ozlem" sort="Dalm Zrak, Ozlem" uniqKey="Dalm Zrak O" first="Özlem" last="Dalm Zrak">Özlem Dalm Zrak</name><affiliation><mods:affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</mods:affiliation></affiliation></author><author><name sortKey="Ercan, Ayse" sort="Ercan, Ayse" uniqKey="Ercan A" first="Ayse" last="Ercan">Ayse Ercan</name><affiliation><mods:affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</mods:affiliation></affiliation></author><author><name sortKey="Kulaks Z, Gulnihal" sort="Kulaks Z, Gulnihal" uniqKey="Kulaks Z G" first="Gülnihal" last="Kulaks Z">Gülnihal Kulaks Z</name><affiliation><mods:affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</mods:affiliation></affiliation></author><author><name sortKey="Ogus, Hamdi" sort="Ogus, Hamdi" uniqKey="Ogus H" first="Hamdi" last="Ögüs">Hamdi Ögüs</name><affiliation><mods:affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</mods:affiliation></affiliation></author><author><name sortKey="Dalkara, Turgay" sort="Dalkara, Turgay" uniqKey="Dalkara T" first="Turgay" last="Dalkara">Turgay Dalkara</name><affiliation><mods:affiliation>Department of Neurology, Hacettepe University, Faculty of Medicine, Ankara, Turkey</mods:affiliation></affiliation></author><author><name sortKey="Ozer, Nazmi" sort="Ozer, Nazmi" uniqKey="Ozer N" first="Nazmi" last="Özer">Nazmi Özer</name><affiliation><mods:affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. 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="2004-05">2004-05</date><biblScope unit="vol">19</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="544">544</biblScope><biblScope unit="page" to="548">548</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">FCC69B357943B6FD8B6B059446C76F8D185770F4</idno><idno type="DOI">10.1002/mds.10695</idno><idno type="ArticleID">MDS10695</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>complex I</term><term>complex IV</term><term>mtDNA</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The parkin protein functions as a RING‐type ubiquitin protein ligase. Considering the possibility that impaired ubiquitin‐proteosomal system activity may impair antioxidant defenses and enhance oxidative stress, we have investigated the activity of mitochondrial respiratory enzymes in patients with parkin gene mutations. A significant decrease in the leukocyte complex I activity was found both in patients with parkin mutations (62.5%) and idiopathic PD (64.5%) compared with age‐matched controls (P < 0.001). Complex IV activity was also decreased significantly in idiopathic PD patients (60%), but no difference was detected between controls and patients with parkin mutations. © 2003 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Meltem Müftüoglu PhD</name><affiliations><json:string>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</json:string></affiliations></json:item><json:item><name>Bülent Elibol MD, PhD</name><affiliations><json:string>Department of Neurology, Hacettepe University, Faculty of Medicine, Ankara, Turkey</json:string></affiliations></json:item><json:item><name>Özlem Dalmızrak MSc</name><affiliations><json:string>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</json:string></affiliations></json:item><json:item><name>Ayse Ercan MSc</name><affiliations><json:string>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</json:string></affiliations></json:item><json:item><name>Gülnihal Kulaksız MD</name><affiliations><json:string>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</json:string></affiliations></json:item><json:item><name>Hamdi Ögüs MD, PhD</name><affiliations><json:string>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</json:string></affiliations></json:item><json:item><name>Turgay Dalkara MD, PhD</name><affiliations><json:string>Department of Neurology, Hacettepe University, Faculty of Medicine, Ankara, Turkey</json:string></affiliations></json:item><json:item><name>Nazmi Özer PhD</name><affiliations><json:string>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>complex I</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>complex IV</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>mtDNA</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The parkin protein functions as a RING‐type ubiquitin protein ligase. Considering the possibility that impaired ubiquitin‐proteosomal system activity may impair antioxidant defenses and enhance oxidative stress, we have investigated the activity of mitochondrial respiratory enzymes in patients with parkin gene mutations. A significant decrease in the leukocyte complex I activity was found both in patients with parkin mutations (62.5%) and idiopathic PD (64.5%) compared with age‐matched controls (P > 0.001). Complex IV activity was also decreased significantly in idiopathic PD patients (60%), but no difference was detected between controls and patients with parkin mutations. © 2003 Movement Disorder Society</abstract><qualityIndicators><score>6.188</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>715</abstractCharCount><pdfWordCount>21179</pdfWordCount><pdfCharCount>134919</pdfCharCount><pdfPageCount>36</pdfPageCount><abstractWordCount>99</abstractWordCount></qualityIndicators><title>Mitochondrial complex I and IV activities in leukocytes from patients with parkin mutations</title><genre><json:string>Serial article</json:string></genre><host><volume>19</volume><pages><total>5</total><last>548</last><first>544</first></pages><issn><json:string>0885-3185</json:string></issn><issue>5</issue><subject><json:item><value>Brief Report</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2004</publicationDate><copyrightDate>2004</copyrightDate><doi><json:string>10.1002/mds.10695</json:string></doi><id>FCC69B357943B6FD8B6B059446C76F8D185770F4</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/FCC69B357943B6FD8B6B059446C76F8D185770F4/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/FCC69B357943B6FD8B6B059446C76F8D185770F4/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/FCC69B357943B6FD8B6B059446C76F8D185770F4/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Mitochondrial complex I and IV activities in leukocytes from patients with parkin mutations</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>2004</date></publicationStmt><notesStmt><note>Scientific and Technical Research Council of Turkey - No. SBAG‐2596; No. TBAG‐1754;</note><note>Hacettepe University Scientific Research Unit - No. 0002101001;</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Mitochondrial complex I and IV activities in leukocytes from patients with parkin mutations</title><author><persName><forename type="first">Meltem</forename><surname>Müftüoglu</surname><roleName type="degree">PhD</roleName></persName><affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation></author><author><persName><forename type="first">Bülent</forename><surname>Elibol</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Department of Neurology, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation></author><author><persName><forename type="first">Özlem</forename><surname>Dalmızrak</surname><roleName type="degree">MSc</roleName></persName><affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation></author><author><persName><forename type="first">Ayse</forename><surname>Ercan</surname><roleName type="degree">MSc</roleName></persName><affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation></author><author><persName><forename type="first">Gülnihal</forename><surname>Kulaksız</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation></author><author><persName><forename type="first">Hamdi</forename><surname>Ögüs</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation></author><author><persName><forename type="first">Turgay</forename><surname>Dalkara</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Department of Neurology, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation></author><author><persName><forename type="first">Nazmi</forename><surname>Özer</surname><roleName type="degree">PhD</roleName></persName><note type="correspondence"><p>Correspondence: Hacettepe University, Faculty of Medicine, Department of Biochemistry, 06100, Sıhhiye, Ankara, Turkey</p></note><affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2004-05"></date><biblScope unit="vol">19</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="544">544</biblScope><biblScope unit="page" to="548">548</biblScope></imprint></monogr><idno type="istex">FCC69B357943B6FD8B6B059446C76F8D185770F4</idno><idno type="DOI">10.1002/mds.10695</idno><idno type="ArticleID">MDS10695</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2004</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The parkin protein functions as a RING‐type ubiquitin protein ligase. Considering the possibility that impaired ubiquitin‐proteosomal system activity may impair antioxidant defenses and enhance oxidative stress, we have investigated the activity of mitochondrial respiratory enzymes in patients with parkin gene mutations. A significant decrease in the leukocyte complex I activity was found both in patients with parkin mutations (62.5%) and idiopathic PD (64.5%) compared with age‐matched controls (P < 0.001). Complex IV activity was also decreased significantly in idiopathic PD patients (60%), but no difference was detected between controls and patients with parkin mutations. © 2003 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>complex I</term></item><item><term>complex IV</term></item><item><term>mtDNA</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Brief Report</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2003-06-05">Received</change><change when="2003-09-23">Registration</change><change when="2004-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/FCC69B357943B6FD8B6B059446C76F8D185770F4/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="50"><doi origin="wiley" registered="yes">10.1002/mds.v19:5</doi><numberingGroup><numbering type="journalVolume" number="19">19</numbering><numbering type="journalIssue">5</numbering></numberingGroup><coverDate startDate="2004-05">May 2004</coverDate></publicationMeta><publicationMeta level="unit" type="shortCommunication" position="80" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.10695</doi><idGroup><id type="unit" value="MDS10695"></id></idGroup><countGroup><count type="pageTotal" number="5"></count></countGroup><titleGroup><title type="articleCategory">Brief Report</title><title type="tocHeading1">Brief Reports</title></titleGroup><copyright ownership="thirdParty">Copyright © 2003 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2003-06-05"></event><event type="manuscriptRevised" date="2003-09-23"></event><event type="manuscriptAccepted" date="2003-09-23"></event><event type="publishedOnlineEarlyUnpaginated" date="2003-12-15"></event><event type="firstOnline" date="2003-12-15"></event><event type="publishedOnlineFinalForm" date="2004-05-03"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-09"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">544</numbering><numbering type="pageLast">548</numbering></numberingGroup><correspondenceTo>Hacettepe University, Faculty of Medicine, Department of Biochemistry, 06100, Sıhhiye, Ankara, Turkey</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS10695.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="32"></count><count type="wordTotal" number="3132"></count></countGroup><titleGroup><title type="main" xml:lang="en">Mitochondrial complex I and IV activities in leukocytes from patients with parkin mutations</title><title type="short" xml:lang="en">Mitochondrial Enyzmes in Parkinson's Disease</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Meltem</givenNames><familyName>Müftüoglu</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Bülent</givenNames><familyName>Elibol</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Özlem</givenNames><familyName>Dalmızrak</familyName><degrees>MSc</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Ayse</givenNames><familyName>Ercan</familyName><degrees>MSc</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Gülnihal</givenNames><familyName>Kulaksız</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Hamdi</givenNames><familyName>Ögüs</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Turgay</givenNames><familyName>Dalkara</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Nazmi</givenNames><familyName>Özer</familyName><degrees>PhD</degrees></personName><contactDetails><email>naozer@hacettepe.edu.tr</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="TR" type="organization"><unparsedAffiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="TR" type="organization"><unparsedAffiliation>Department of Neurology, Hacettepe University, Faculty of Medicine, Ankara, Turkey</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">complex I</keyword><keyword xml:id="kwd3">complex IV</keyword><keyword xml:id="kwd4">mtDNA</keyword></keywordGroup><fundingInfo><fundingAgency>Scientific and Technical Research Council of Turkey</fundingAgency><fundingNumber>SBAG‐2596</fundingNumber><fundingNumber>TBAG‐1754</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Hacettepe University Scientific Research Unit</fundingAgency><fundingNumber>0002101001</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The parkin protein functions as a RING‐type ubiquitin protein ligase. Considering the possibility that impaired ubiquitin‐proteosomal system activity may impair antioxidant defenses and enhance oxidative stress, we have investigated the activity of mitochondrial respiratory enzymes in patients with parkin gene mutations. A significant decrease in the leukocyte complex I activity was found both in patients with parkin mutations (62.5%) and idiopathic PD (64.5%) compared with age‐matched controls (<i>P</i> < 0.001). Complex IV activity was also decreased significantly in idiopathic PD patients (60%), but no difference was detected between controls and patients with parkin mutations. © 2003 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Mitochondrial complex I and IV activities in leukocytes from patients with parkin mutations</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Mitochondrial Enyzmes in Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Mitochondrial complex I and IV activities in leukocytes from patients with parkin mutations</title></titleInfo><name type="personal"><namePart type="given">Meltem</namePart><namePart type="family">Müftüoglu</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bülent</namePart><namePart type="family">Elibol</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Özlem</namePart><namePart type="family">Dalmızrak</namePart><namePart type="termsOfAddress">MSc</namePart><affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ayse</namePart><namePart type="family">Ercan</namePart><namePart type="termsOfAddress">MSc</namePart><affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gülnihal</namePart><namePart type="family">Kulaksız</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hamdi</namePart><namePart type="family">Ögüs</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Turgay</namePart><namePart type="family">Dalkara</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nazmi</namePart><namePart type="family">Özer</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation><description>Correspondence: Hacettepe University, Faculty of Medicine, Department of Biochemistry, 06100, Sıhhiye, Ankara, Turkey</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">shortCommunication</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2004-05</dateIssued><dateCaptured encoding="w3cdtf">2003-06-05</dateCaptured><dateValid encoding="w3cdtf">2003-09-23</dateValid><copyrightDate encoding="w3cdtf">2004</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">3</extent><extent unit="tables">2</extent><extent unit="references">32</extent><extent unit="words">3132</extent></physicalDescription><abstract lang="en">The parkin protein functions as a RING‐type ubiquitin protein ligase. Considering the possibility that impaired ubiquitin‐proteosomal system activity may impair antioxidant defenses and enhance oxidative stress, we have investigated the activity of mitochondrial respiratory enzymes in patients with parkin gene mutations. A significant decrease in the leukocyte complex I activity was found both in patients with parkin mutations (62.5%) and idiopathic PD (64.5%) compared with age‐matched controls (P < 0.001). Complex IV activity was also decreased significantly in idiopathic PD patients (60%), but no difference was detected between controls and patients with parkin mutations. © 2003 Movement Disorder Society</abstract><note type="funding">Scientific and Technical Research Council of Turkey - No. SBAG‐2596; No. TBAG‐1754; </note><note type="funding">Hacettepe University Scientific Research Unit - No. 0002101001; </note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>complex I</topic><topic>complex IV</topic><topic>mtDNA</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Brief Report</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>19</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>544</start><end>548</end><total>5</total></extent></part></relatedItem><identifier type="istex">FCC69B357943B6FD8B6B059446C76F8D185770F4</identifier><identifier type="DOI">10.1002/mds.10695</identifier><identifier type="ArticleID">MDS10695</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2003 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001577 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 001577 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Santé
|area= MovDisordV3
|flux= Istex
|étape= Corpus
|type= RBID
|clé= ISTEX:FCC69B357943B6FD8B6B059446C76F8D185770F4
|texte= Mitochondrial complex I and IV activities in leukocytes from patients with parkin mutations
}}
| This area was generated with Dilib version V0.6.23. |  |