p53 in neurodegenerative diseases and brain cancers
Identifieur interne : 000A94 ( Main/Exploration ); précédent : 000A93; suivant : 000A95p53 in neurodegenerative diseases and brain cancers
Auteurs : Frédéric Checler [France] ; Cristine Alves Da Costa [France]Source :
- Pharmacology & therapeutics : (Oxford) [ 0163-7258 ] ; 2014.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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.
Affiliations:
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Pharmacologie Moléculaire et Cellulaire, UMR7275 CNRS/UNS, "Labex Distalz", 660 route des Lucioles</s1><s2>06560, Sophia-Antipolis, Valbonne</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>France</country><wicri:noRegion>Valbonne</wicri:noRegion><wicri:noRegion>660 route des Lucioles</wicri:noRegion><wicri:noRegion>06560, Sophia-Antipolis, Valbonne</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">14-0117814</idno><date when="2014">2014</date><idno type="stanalyst">PASCAL 14-0117814 INIST</idno><idno type="RBID">Pascal:14-0117814</idno><idno type="wicri:Area/PascalFrancis/Corpus">000036</idno><idno type="stanalyst">FRANCIS 14-0117814 INIST</idno><idno type="wicri:Area/PascalFrancis/Corpus">000068</idno><idno type="wicri:Area/PascalFrancis/Curation">001245</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000012</idno><idno type="wicri:explorRef" wicri:stream="PascalFrancis" 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Valbonne</wicri:noRegion></affiliation></author><author><name sortKey="Da Costa, Cristine Alves" sort="Da Costa, Cristine Alves" uniqKey="Da Costa C" first="Cristine Alves" last="Da Costa">Cristine Alves Da Costa</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Institut de Pharmacologie Moléculaire et Cellulaire, UMR7275 CNRS/UNS, "Labex Distalz", 660 route des Lucioles</s1><s2>06560, Sophia-Antipolis, Valbonne</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>France</country><wicri:noRegion>Valbonne</wicri:noRegion><wicri:noRegion>660 route des Lucioles</wicri:noRegion><wicri:noRegion>06560, Sophia-Antipolis, Valbonne</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Pharmacology & therapeutics : (Oxford)</title><title level="j" type="abbreviated">Pharmacol. ther. : (Oxf.)</title><idno type="ISSN">0163-7258</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Pharmacology & therapeutics : (Oxford)</title><title level="j" type="abbreviated">Pharmacol. ther. : (Oxf.)</title><idno type="ISSN">0163-7258</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alzheimer disease</term><term>Brain cancer</term><term>Cerebral disorder</term><term>Degenerative disease</term><term>Encephalon</term><term>Malignant tumor</term><term>Nervous system diseases</term><term>Parkinson disease</term><term>Signal transduction</term><term>TP53 Gene</term><term>Treatment</term><term>Tumor suppressor gene</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Gène TP53</term><term>Gène suppresseur tumeur</term><term>Maladie dégénérative</term><term>Pathologie du système nerveux</term><term>Pathologie de l'encéphale</term><term>Cancer du cerveau</term><term>Transduction signal</term><term>Démence d'Alzheimer</term><term>Maladie de Parkinson</term><term>Encéphale</term><term>Tumeur maligne</term><term>Traitement</term><term>Gène p53</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><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="Da Costa, Cristine Alves" sort="Da Costa, Cristine Alves" uniqKey="Da Costa C" first="Cristine Alves" last="Da Costa">Cristine Alves Da Costa</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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