DJ‐1, PINK1, and their effects on mitochondrial pathways
Identifieur interne : 001D67 ( Main/Exploration ); précédent : 001D66; suivant : 001D68DJ‐1, PINK1, and their effects on mitochondrial pathways
Auteurs : Mark R. Cookson [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2010.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Animals, DJ‐1, Genetic Predisposition to Disease, Humans, Intracellular Signaling Peptides and Proteins (genetics), Intracellular Signaling Peptides and Proteins (metabolism), Mitochondria, Mitochondria (genetics), Mitochondria (metabolism), Mitochondria (pathology), Nervous system diseases, Oncogene Proteins (genetics), Oncogene Proteins (metabolism), Oxidative Stress (physiology), PINK1, Parkin, Parkinsonian Disorders (genetics), Parkinsonian Disorders (metabolism), Parkinsonian Disorders (pathology), Parkinsonism, Protein Kinases (genetics), Protein Kinases (metabolism), genetics, parkin, parkinsonism.
- MESH :
- chemical , genetics : Intracellular Signaling Peptides and Proteins, Oncogene Proteins, Protein Kinases.
- chemical , metabolism : Intracellular Signaling Peptides and Proteins, Oncogene Proteins, Protein Kinases.
- genetics : Mitochondria, Parkinsonian Disorders.
- metabolism : Mitochondria, Parkinsonian Disorders.
- pathology : Mitochondria, Parkinsonian Disorders.
- physiology : Oxidative Stress.
- Animals, Genetic Predisposition to Disease, Humans.
Abstract
Genetic forms of parkinsonism are interesting for two particular reasons. First, finding a gene identifies a cause for a disease that would otherwise be unexplained. Second, finding several genes for the same disorder allows us to reconstruct molecular pathways that, in the example of Parkinson's disease, are be associated with the survival of dopamine neurons in the substantia nigra. Two rare causes of parkinsonism, DJ‐1 and PINK1, are associated with mitochondria. This organelle has long been linked with Parkinson's disease, and recent results are starting to show how mutations impact mitochondrial function. In this short review, I will discuss how we can use some of this information to understand why it is that neurons become dysfunctional in PD. © 2010 Movement Disorder Society
Url:
- https://api.istex.fr/document/AB427D4E84101BD7B956FEBA09627EF2870C9754/fulltext/pdf
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2840196
DOI: 10.1002/mds.22713
Affiliations:
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Le document en format XML
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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="2010">2010</date><biblScope unit="vol">25</biblScope><biblScope unit="issue">S1</biblScope><biblScope unit="page" from="S44">S44</biblScope><biblScope unit="page" to="S48">S48</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">AB427D4E84101BD7B956FEBA09627EF2870C9754</idno><idno type="DOI">10.1002/mds.22713</idno><idno type="ArticleID">MDS22713</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>DJ‐1</term><term>Genetic Predisposition to Disease</term><term>Humans</term><term>Intracellular Signaling Peptides and Proteins (genetics)</term><term>Intracellular Signaling Peptides and Proteins (metabolism)</term><term>Mitochondria</term><term>Mitochondria (genetics)</term><term>Mitochondria (metabolism)</term><term>Mitochondria (pathology)</term><term>Nervous system diseases</term><term>Oncogene Proteins (genetics)</term><term>Oncogene Proteins (metabolism)</term><term>Oxidative Stress (physiology)</term><term>PINK1</term><term>Parkin</term><term>Parkinsonian Disorders (genetics)</term><term>Parkinsonian Disorders (metabolism)</term><term>Parkinsonian Disorders (pathology)</term><term>Parkinsonism</term><term>Protein Kinases (genetics)</term><term>Protein Kinases (metabolism)</term><term>genetics</term><term>parkin</term><term>parkinsonism</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Intracellular Signaling Peptides and Proteins</term><term>Oncogene Proteins</term><term>Protein Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Intracellular Signaling Peptides and Proteins</term><term>Oncogene Proteins</term><term>Protein Kinases</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mitochondria</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Mitochondria</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Mitochondria</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Oxidative Stress</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Genetic Predisposition to Disease</term><term>Humans</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Mitochondrie</term><term>Parkine</term><term>Parkinsonisme</term><term>Pathologie du système nerveux</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Genetic forms of parkinsonism are interesting for two particular reasons. First, finding a gene identifies a cause for a disease that would otherwise be unexplained. Second, finding several genes for the same disorder allows us to reconstruct molecular pathways that, in the example of Parkinson's disease, are be associated with the survival of dopamine neurons in the substantia nigra. Two rare causes of parkinsonism, DJ‐1 and PINK1, are associated with mitochondria. This organelle has long been linked with Parkinson's disease, and recent results are starting to show how mutations impact mitochondrial function. In this short review, I will discuss how we can use some of this information to understand why it is that neurons become dysfunctional in PD. © 2010 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li></region></list><tree><country name="États-Unis"><region name="Maryland"><name sortKey="Cookson, Mark R" sort="Cookson, Mark R" uniqKey="Cookson M" first="Mark R." last="Cookson">Mark R. Cookson</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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