Apoptosis in Parkinson's disease: is p53 the missing link between genetic and sporadic Parkinsonism?
Identifieur interne : 000934 ( PubMed/Checkpoint ); précédent : 000933; suivant : 000935Apoptosis in Parkinson's disease: is p53 the missing link between genetic and sporadic Parkinsonism?
Auteurs : Cristine Alves Da Costa [France] ; Frédéric CheclerSource :
- Cellular signalling [ 1873-3913 ] ; 2011.
English descriptors
- KwdEn :
- Animals, Apoptosis, Autophagy, Disease Models, Animal, Genes, Recessive, Humans, Intracellular Signaling Peptides and Proteins (genetics), Intracellular Signaling Peptides and Proteins (metabolism), Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, Oncogene Proteins (genetics), Oncogene Proteins (metabolism), Parkinson Disease (drug therapy), Parkinson Disease (etiology), Parkinson Disease (pathology), Protein Deglycase DJ-1, Protein Kinases (genetics), Protein Kinases (metabolism), Protein-Serine-Threonine Kinases (genetics), Protein-Serine-Threonine Kinases (metabolism), Tumor Suppressor Protein p53 (metabolism), Ubiquitin-Protein Ligases (genetics), Ubiquitin-Protein Ligases (metabolism), alpha-Synuclein (genetics), alpha-Synuclein (metabolism).
- MESH :
- chemical , genetics : Intracellular Signaling Peptides and Proteins, Oncogene Proteins, Protein Kinases, Protein-Serine-Threonine Kinases, Ubiquitin-Protein Ligases, alpha-Synuclein.
- chemical , metabolism : Intracellular Signaling Peptides and Proteins, Oncogene Proteins, Protein Kinases, Protein-Serine-Threonine Kinases, Tumor Suppressor Protein p53, Ubiquitin-Protein Ligases, alpha-Synuclein.
- drug therapy : Parkinson Disease.
- etiology : Parkinson Disease.
- pathology : Parkinson Disease.
- Animals, Apoptosis, Autophagy, Disease Models, Animal, Genes, Recessive, Humans, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, Protein Deglycase DJ-1.
Abstract
Parkinson's disease (PD) is a major age-related neurodegenerative disorder characterized by a massive and specific loss of dopaminergic neurons of the substantia nigra pars compacta. The cellular alterations are clinically translated into an invalidating movement disability associated to three canonical symptoms that are bradykinesia, resting tremor and rigidity. The exact causes of this neuronal loss are unknown, but a network of evidences indicates a major contribution of orchestrated cell death processes, also known as apoptosis. Apoptotic cell death is a normal process, the alteration of which triggers several pathologies including cancer and neurodegenerative disorders. Exhaustive work has been done to delineate the cellular mechanisms responsible for the exacerbated cell death of dopaminergic neurons observed in PD. Overall, the oncogene p53 has been identified as a key effector protein. This review will focus on the clues linking p53 to the etiology of PD and the evidences that this protein may be at the center of multiple signaling cascades not only altered by mutations of various proteins responsible for familial cases of PD but also on more general sporadic cases of this devastating disease.
DOI: 10.1016/j.cellsig.2010.10.020
PubMed: 20969953
Affiliations:
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type="city">Valbonne</settlement></placeName></affiliation></author><author><name sortKey="Checler, Frederic" sort="Checler, Frederic" uniqKey="Checler F" first="Frédéric" last="Checler">Frédéric Checler</name></author></analytic><series><title level="j">Cellular signalling</title><idno type="eISSN">1873-3913</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Autophagy</term><term>Disease Models, Animal</term><term>Genes, Recessive</term><term>Humans</term><term>Intracellular Signaling Peptides and Proteins (genetics)</term><term>Intracellular Signaling Peptides and Proteins (metabolism)</term><term>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</term><term>Oncogene Proteins (genetics)</term><term>Oncogene Proteins (metabolism)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease 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Proteins</term><term>Protein Kinases</term><term>Protein-Serine-Threonine Kinases</term><term>Tumor Suppressor Protein p53</term><term>Ubiquitin-Protein Ligases</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Autophagy</term><term>Disease Models, Animal</term><term>Genes, Recessive</term><term>Humans</term><term>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</term><term>Protein Deglycase DJ-1</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a major age-related neurodegenerative disorder characterized by a massive and specific loss of dopaminergic neurons of the substantia nigra pars compacta. The cellular alterations are clinically translated into an invalidating movement disability associated to three canonical symptoms that are bradykinesia, resting tremor and rigidity. The exact causes of this neuronal loss are unknown, but a network of evidences indicates a major contribution of orchestrated cell death processes, also known as apoptosis. Apoptotic cell death is a normal process, the alteration of which triggers several pathologies including cancer and neurodegenerative disorders. Exhaustive work has been done to delineate the cellular mechanisms responsible for the exacerbated cell death of dopaminergic neurons observed in PD. Overall, the oncogene p53 has been identified as a key effector protein. This review will focus on the clues linking p53 to the etiology of PD and the evidences that this protein may be at the center of multiple signaling cascades not only altered by mutations of various proteins responsible for familial cases of PD but also on more general sporadic cases of this devastating disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20969953</PMID><DateCreated><Year>2011</Year><Month>03</Month><Day>22</Day></DateCreated><DateCompleted><Year>2011</Year><Month>06</Month><Day>27</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-3913</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>6</Issue><PubDate><Year>2011</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Cellular signalling</Title><ISOAbbreviation>Cell. 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Apoptotic cell death is a normal process, the alteration of which triggers several pathologies including cancer and neurodegenerative disorders. Exhaustive work has been done to delineate the cellular mechanisms responsible for the exacerbated cell death of dopaminergic neurons observed in PD. Overall, the oncogene p53 has been identified as a key effector protein. This review will focus on the clues linking p53 to the etiology of PD and the evidences that this protein may be at the center of multiple signaling cascades not only altered by mutations of various proteins responsible for familial cases of PD but also on more general sporadic cases of this devastating disease.</AbstractText><CopyrightInformation>Copyright © 2010 Elsevier Inc. 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UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2010</Year><Month>09</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2010</Year><Month>10</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2010</Year><Month>10</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2010</Year><Month>10</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>6</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">20969953</ArticleId><ArticleId IdType="pii">S0898-6568(10)00307-4</ArticleId><ArticleId IdType="doi">10.1016/j.cellsig.2010.10.020</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Provence-Alpes-Côte d'Azur</li></region><settlement><li>Valbonne</li></settlement></list><tree><noCountry><name sortKey="Checler, Frederic" sort="Checler, Frederic" uniqKey="Checler F" first="Frédéric" last="Checler">Frédéric Checler</name></noCountry><country name="France"><region name="Provence-Alpes-Côte d'Azur"><name sortKey="Alves Da Costa, Cristine" sort="Alves Da Costa, Cristine" uniqKey="Alves Da Costa C" first="Cristine" last="Alves Da Costa">Cristine Alves Da Costa</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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