Parkin counteracts symptoms in a Drosophila model of Parkinson's disease.
Identifieur interne : 001351 ( PubMed/Corpus ); précédent : 001350; suivant : 001352Parkin counteracts symptoms in a Drosophila model of Parkinson's disease.
Auteurs : Annika F M. Haywood ; Brian E. StaveleySource :
- BMC neuroscience [ 1471-2202 ] ; 2004.
English descriptors
- KwdEn :
- Amino Acid Sequence, Animals, Animals, Genetically Modified, Behavior, Animal, Conserved Sequence (genetics), Disease Models, Animal, Dopamine (metabolism), Drosophila Proteins (biosynthesis), Drosophila Proteins (genetics), Drosophila Proteins (physiology), Drosophila melanogaster, Gene Transfer Techniques, Genetic Therapy, Humans, Molecular Sequence Data, Nerve Tissue Proteins (genetics), Nerve Tissue Proteins (metabolism), Neurons (metabolism), Parkinson Disease (complications), Parkinson Disease (genetics), Parkinson Disease (therapy), Retinal Degeneration (genetics), Retinal Degeneration (pathology), Retinal Degeneration (therapy), Sequence Homology, Amino Acid, Survival Rate, Synucleins, Ubiquitin-Protein Ligases, alpha-Synuclein.
- MESH :
- chemical , biosynthesis : Drosophila Proteins.
- chemical , genetics : Drosophila Proteins, Nerve Tissue Proteins.
- chemical , metabolism : Dopamine, Nerve Tissue Proteins.
- complications : Parkinson Disease.
- genetics : Conserved Sequence, Parkinson Disease, Retinal Degeneration.
- metabolism : Neurons.
- pathology : Retinal Degeneration.
- chemical , physiology : Drosophila Proteins.
- therapy : Parkinson Disease, Retinal Degeneration.
- Amino Acid Sequence, Animals, Animals, Genetically Modified, Behavior, Animal, Disease Models, Animal, Drosophila melanogaster, Gene Transfer Techniques, Genetic Therapy, Humans, Molecular Sequence Data, Sequence Homology, Amino Acid, Survival Rate, Synucleins, Ubiquitin-Protein Ligases, alpha-Synuclein.
Abstract
Parkinson's disease, a prevalent neurodegenerative disease, is characterized by the reduction of dopaminergic neurons resulting in the loss of motor control, resting tremor, the formation of neuronal inclusions and ultimately premature death. Two inherited forms of PD have been linked to mutations in the alpha-synuclein and parkin genes. The parkin protein functions as an ubiquitin ligase targeting specific proteins for degradation. Expression of human alpha-synuclein in Drosophila neurons recapitulates the loss of motor control, the development of neuronal inclusions, degeneration of dopaminergic neurons and the ommatidial array to provide an excellent genetic model of PD.
DOI: 10.1186/1471-2202-5-14
PubMed: 15090075
Links to Exploration step
pubmed:15090075Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Parkin counteracts symptoms in a Drosophila model of Parkinson's disease.</title><author><name sortKey="Haywood, Annika F M" sort="Haywood, Annika F M" uniqKey="Haywood A" first="Annika F M" last="Haywood">Annika F M. Haywood</name><affiliation><nlm:affiliation>Department of Biology, Memorial University of Newfoundland, St John's, Newfoundland and Labrador, A1B 3X9, Canada. annikahaywood@warp.nfld.net</nlm:affiliation></affiliation></author><author><name sortKey="Staveley, Brian E" sort="Staveley, Brian E" uniqKey="Staveley B" first="Brian E" last="Staveley">Brian E. Staveley</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2004">2004</date><idno type="RBID">pubmed:15090075</idno><idno type="pmid">15090075</idno><idno type="doi">10.1186/1471-2202-5-14</idno><idno type="wicri:Area/PubMed/Corpus">001351</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001351</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Parkin counteracts symptoms in a Drosophila model of Parkinson's disease.</title><author><name sortKey="Haywood, Annika F M" sort="Haywood, Annika F M" uniqKey="Haywood A" first="Annika F M" last="Haywood">Annika F M. Haywood</name><affiliation><nlm:affiliation>Department of Biology, Memorial University of Newfoundland, St John's, Newfoundland and Labrador, A1B 3X9, Canada. annikahaywood@warp.nfld.net</nlm:affiliation></affiliation></author><author><name sortKey="Staveley, Brian E" sort="Staveley, Brian E" uniqKey="Staveley B" first="Brian E" last="Staveley">Brian E. Staveley</name></author></analytic><series><title level="j">BMC neuroscience</title><idno type="eISSN">1471-2202</idno><imprint><date when="2004" type="published">2004</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amino Acid Sequence</term><term>Animals</term><term>Animals, Genetically Modified</term><term>Behavior, Animal</term><term>Conserved Sequence (genetics)</term><term>Disease Models, Animal</term><term>Dopamine (metabolism)</term><term>Drosophila Proteins (biosynthesis)</term><term>Drosophila Proteins (genetics)</term><term>Drosophila Proteins (physiology)</term><term>Drosophila melanogaster</term><term>Gene Transfer Techniques</term><term>Genetic Therapy</term><term>Humans</term><term>Molecular Sequence Data</term><term>Nerve Tissue Proteins (genetics)</term><term>Nerve Tissue Proteins (metabolism)</term><term>Neurons (metabolism)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (therapy)</term><term>Retinal Degeneration (genetics)</term><term>Retinal Degeneration (pathology)</term><term>Retinal Degeneration (therapy)</term><term>Sequence Homology, Amino Acid</term><term>Survival Rate</term><term>Synucleins</term><term>Ubiquitin-Protein Ligases</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Drosophila Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Drosophila Proteins</term><term>Nerve Tissue Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>Nerve Tissue Proteins</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Conserved Sequence</term><term>Parkinson Disease</term><term>Retinal Degeneration</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Retinal Degeneration</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Drosophila Proteins</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term><term>Retinal Degeneration</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Amino Acid Sequence</term><term>Animals</term><term>Animals, Genetically Modified</term><term>Behavior, Animal</term><term>Disease Models, Animal</term><term>Drosophila melanogaster</term><term>Gene Transfer Techniques</term><term>Genetic Therapy</term><term>Humans</term><term>Molecular Sequence Data</term><term>Sequence Homology, Amino Acid</term><term>Survival Rate</term><term>Synucleins</term><term>Ubiquitin-Protein Ligases</term><term>alpha-Synuclein</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease, a prevalent neurodegenerative disease, is characterized by the reduction of dopaminergic neurons resulting in the loss of motor control, resting tremor, the formation of neuronal inclusions and ultimately premature death. Two inherited forms of PD have been linked to mutations in the alpha-synuclein and parkin genes. The parkin protein functions as an ubiquitin ligase targeting specific proteins for degradation. Expression of human alpha-synuclein in Drosophila neurons recapitulates the loss of motor control, the development of neuronal inclusions, degeneration of dopaminergic neurons and the ommatidial array to provide an excellent genetic model of PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15090075</PMID><DateCreated><Year>2004</Year><Month>05</Month><Day>26</Day></DateCreated><DateCompleted><Year>2004</Year><Month>07</Month><Day>09</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1471-2202</ISSN><JournalIssue CitedMedium="Internet"><Volume>5</Volume><PubDate><Year>2004</Year><Month>Apr</Month><Day>16</Day></PubDate></JournalIssue><Title>BMC neuroscience</Title><ISOAbbreviation>BMC Neurosci</ISOAbbreviation></Journal><ArticleTitle>Parkin counteracts symptoms in a Drosophila model of Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>14</MedlinePgn></Pagination><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Parkinson's disease, a prevalent neurodegenerative disease, is characterized by the reduction of dopaminergic neurons resulting in the loss of motor control, resting tremor, the formation of neuronal inclusions and ultimately premature death. Two inherited forms of PD have been linked to mutations in the alpha-synuclein and parkin genes. The parkin protein functions as an ubiquitin ligase targeting specific proteins for degradation. Expression of human alpha-synuclein in Drosophila neurons recapitulates the loss of motor control, the development of neuronal inclusions, degeneration of dopaminergic neurons and the ommatidial array to provide an excellent genetic model of PD.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">To investigate the role of parkin, we have generated transgenic Drosophila that conditionally express parkin under the control of the yeast UAS enhancer. While expression of parkin has little consequence, co-expression of parkin with alpha-synuclein in the dopaminergic neurons suppresses the alpha-synuclein-induced premature loss of climbing ability. In addition directed expression of parkin in the eye counteracts the alpha-synuclein-induced degeneration of the ommatidial array. These results show that parkin suppresses the PD-like symptoms observed in the alpha-synuclein-dependent Drosophila model of PD.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">The highly conserved parkin E3 ubiquitin ligase can suppress the damaging effects of human alpha-synuclein. These results are consistent with a role for parkin in targeting alpha-synuclein to the proteasome. If this relationship is conserved in humans, this suggests that up-regulation of parkin should suppress alpha-synucleinopathic PD. The development of therapies that regulate parkin activity may be crucial in the treatment of PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Haywood</LastName><ForeName>Annika F M</ForeName><Initials>AF</Initials><AffiliationInfo><Affiliation>Department of Biology, Memorial University of Newfoundland, St John's, Newfoundland and Labrador, A1B 3X9, Canada. annikahaywood@warp.nfld.net</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Staveley</LastName><ForeName>Brian E</ForeName><Initials>BE</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2004</Year><Month>04</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC 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Drosophila</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>J Mol Med (Berl). 2001 Sep;79(9):482-94</RefSource><PMID Version="1">11692161</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochem Biophys Res Commun. 2003 Sep 26;309(3):679-84</RefSource><PMID Version="1">12963044</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Annu Rev Biochem. 2001;70:503-33</RefSource><PMID Version="1">11395416</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 2002 Feb 1;295(5556):865-8</RefSource><PMID Version="1">11823645</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2002 Apr 15;22(8):3090-9</RefSource><PMID 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MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029721" MajorTopicYN="N">Drosophila Proteins</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004331" MajorTopicYN="Y">Drosophila melanogaster</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018014" MajorTopicYN="N">Gene Transfer Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015316" MajorTopicYN="N">Genetic Therapy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008969" MajorTopicYN="N">Molecular Sequence Data</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009419" MajorTopicYN="N">Nerve Tissue Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000628" 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