p53 in neurodegenerative diseases and brain cancers.
Identifieur interne : 000424 ( PubMed/Checkpoint ); précédent : 000423; suivant : 000425p53 in neurodegenerative diseases and brain cancers.
Auteurs : Frédéric Checler [France] ; Cristine Alves Da Costa [France]Source :
- Pharmacology & therapeutics [ 1879-016X ] ; 2014.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Tumor Suppressor Protein p53.
- chemical : Prions.
- genetics : Brain Neoplasms, Neurodegenerative Diseases.
- metabolism : Brain Neoplasms, Neurodegenerative Diseases.
- therapy : Brain Neoplasms, Neurodegenerative Diseases.
- Animals, Genetic Therapy, Humans.
Abstract
More than thirty years elapsed since a protein, not yet called p53 at the time, was detected to bind SV40 during viral infection. Thousands of papers later, p53 evolved as the main tumor suppressor involved in growth arrest and apoptosis. A lot has been done but the protein has not yet revealed all its secrets. Particularly important is the observation that in totally distinct pathologies where apoptosis is either exacerbated or impaired, p53 appears to play a central role. This is exemplified for Alzheimer's and Parkinson's diseases that represent the two main causes of age-related neurodegenerative affections, where cell death enhancement appears as one of the main etiological paradigms. Conversely, in cancers, about half of the cases are linked to mutations in p53 leading to the impairment of p53-dependent apoptosis. The involvement of p53 in these pathologies has driven a huge amount of studies aimed at designing chemical tools or biological approaches to rescue p53 defects or over-activity. Here, we describe the data linking p53 to neurodegenerative diseases and brain cancers, and we document the various strategies to interfere with p53 dysfunctions in these disorders.
DOI: 10.1016/j.pharmthera.2013.11.009
PubMed: 24287312
Affiliations:
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Thousands of papers later, p53 evolved as the main tumor suppressor involved in growth arrest and apoptosis. A lot has been done but the protein has not yet revealed all its secrets. Particularly important is the observation that in totally distinct pathologies where apoptosis is either exacerbated or impaired, p53 appears to play a central role. This is exemplified for Alzheimer's and Parkinson's diseases that represent the two main causes of age-related neurodegenerative affections, where cell death enhancement appears as one of the main etiological paradigms. Conversely, in cancers, about half of the cases are linked to mutations in p53 leading to the impairment of p53-dependent apoptosis. The involvement of p53 in these pathologies has driven a huge amount of studies aimed at designing chemical tools or biological approaches to rescue p53 defects or over-activity. Here, we describe the data linking p53 to neurodegenerative diseases and brain cancers, and we document the various strategies to interfere with p53 dysfunctions in these disorders.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24287312</PMID><DateCreated><Year>2014</Year><Month>02</Month><Day>28</Day></DateCreated><DateCompleted><Year>2014</Year><Month>10</Month><Day>20</Day></DateCompleted><DateRevised><Year>2014</Year><Month>02</Month><Day>28</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-016X</ISSN><JournalIssue CitedMedium="Internet"><Volume>142</Volume><Issue>1</Issue><PubDate><Year>2014</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Pharmacology & therapeutics</Title><ISOAbbreviation>Pharmacol. Ther.</ISOAbbreviation></Journal><ArticleTitle>p53 in neurodegenerative diseases and brain cancers.</ArticleTitle><Pagination><MedlinePgn>99-113</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.pharmthera.2013.11.009</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0163-7258(13)00227-1</ELocationID><Abstract><AbstractText>More than thirty years elapsed since a protein, not yet called p53 at the time, was detected to bind SV40 during viral infection. Thousands of papers later, p53 evolved as the main tumor suppressor involved in growth arrest and apoptosis. A lot has been done but the protein has not yet revealed all its secrets. Particularly important is the observation that in totally distinct pathologies where apoptosis is either exacerbated or impaired, p53 appears to play a central role. This is exemplified for Alzheimer's and Parkinson's diseases that represent the two main causes of age-related neurodegenerative affections, where cell death enhancement appears as one of the main etiological paradigms. Conversely, in cancers, about half of the cases are linked to mutations in p53 leading to the impairment of p53-dependent apoptosis. The involvement of p53 in these pathologies has driven a huge amount of studies aimed at designing chemical tools or biological approaches to rescue p53 defects or over-activity. Here, we describe the data linking p53 to neurodegenerative diseases and brain cancers, and we document the various strategies to interfere with p53 dysfunctions in these disorders.</AbstractText><CopyrightInformation>Copyright © 2013 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Checler</LastName><ForeName>Frédéric</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Institut de Pharmacologie Moléculaire et Cellulaire, UMR7275 CNRS/UNS, "Labex Distalz", 660 route des Lucioles, 06560, Sophia-Antipolis, Valbonne, France. Electronic address: checler@ipmc.cnrs.fr.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alves da Costa</LastName><ForeName>Cristine</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Institut de Pharmacologie Moléculaire et Cellulaire, UMR7275 CNRS/UNS, "Labex Distalz", 660 route des Lucioles, 06560, Sophia-Antipolis, Valbonne, France. Electronic address: acosta@ipmc.cnrs.fr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>11</Month><Day>25</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Pharmacol Ther</MedlineTA><NlmUniqueID>7905840</NlmUniqueID><ISSNLinking>0163-7258</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011328">Prions</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016159">Tumor Suppressor Protein p53</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001932" MajorTopicYN="N">Brain Neoplasms</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015316" MajorTopicYN="N">Genetic Therapy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019636" MajorTopicYN="N">Neurodegenerative Diseases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011328" MajorTopicYN="N">Prions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016159" MajorTopicYN="N">Tumor Suppressor Protein p53</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Alzheimer's disease</Keyword><Keyword MajorTopicYN="N">Cerebral cancers</Keyword><Keyword MajorTopicYN="N">Parkinson's disease</Keyword><Keyword MajorTopicYN="N">Signaling</Keyword><Keyword MajorTopicYN="N">Therapeutics</Keyword><Keyword MajorTopicYN="N">p53</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year><Month>11</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2013</Year><Month>11</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>11</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>11</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>10</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24287312</ArticleId><ArticleId IdType="pii">S0163-7258(13)00227-1</ArticleId><ArticleId IdType="doi">10.1016/j.pharmthera.2013.11.009</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country></list><tree><country name="France"><noRegion><name sortKey="Checler, Frederic" sort="Checler, Frederic" uniqKey="Checler F" first="Frédéric" last="Checler">Frédéric Checler</name></noRegion><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></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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