The nuclear oncogene SET controls DNA repair by KAP1 and HP1 retention to chromatin.
Identifieur interne : 002719 ( Main/Exploration ); précédent : 002718; suivant : 002720The nuclear oncogene SET controls DNA repair by KAP1 and HP1 retention to chromatin.
Auteurs : Alkmini Kalousi [France] ; Anne-Sophie Hoffbeck [France] ; Platonas N. Selemenakis [Grèce] ; Jordan Pinder [Canada] ; Kienan I. Savage [Australie] ; Kum Kum Khanna [Australie] ; Laurent Brino [France] ; Graham Dellaire [Canada] ; Vassilis G. Gorgoulis [Grèce] ; Evi Soutoglou [France]Source :
- Cell reports [ 2211-1247 ] ; 2015.
Descripteurs français
- KwdFr :
- Altération de l'ADN (génétique), Cassures double-brin de l'ADN (), Chaperons d'histones (antagonistes et inhibiteurs), Chaperons d'histones (génétique), Chaperons d'histones (métabolisme), Chromatine (génétique), Facteurs de transcription (antagonistes et inhibiteurs), Facteurs de transcription (génétique), Facteurs de transcription (métabolisme), Humains, Hétérochromatine (génétique), Protéines chromosomiques nonhistones (biosynthèse), Protéines chromosomiques nonhistones (génétique), Protéines de liaison à l'ADN (génétique), Protéines de répression (biosynthèse), Protéines de répression (génétique), Réparation de l'ADN par recombinaison (génétique).
- MESH :
- antagonistes et inhibiteurs : Chaperons d'histones, Facteurs de transcription.
- biosynthèse : Protéines chromosomiques nonhistones, Protéines de répression.
- génétique : Altération de l'ADN, Chaperons d'histones, Chromatine, Facteurs de transcription, Hétérochromatine, Protéines chromosomiques nonhistones, Protéines de liaison à l'ADN, Protéines de répression, Réparation de l'ADN par recombinaison.
- métabolisme : Chaperons d'histones, Facteurs de transcription.
- Cassures double-brin de l'ADN, Humains.
English descriptors
- KwdEn :
- Chromatin (genetics), Chromosomal Proteins, Non-Histone (biosynthesis), Chromosomal Proteins, Non-Histone (genetics), DNA Breaks, Double-Stranded (drug effects), DNA Damage (genetics), DNA-Binding Proteins (genetics), Heterochromatin (genetics), Histone Chaperones (antagonists & inhibitors), Histone Chaperones (genetics), Histone Chaperones (metabolism), Humans, Recombinational DNA Repair (genetics), Repressor Proteins (biosynthesis), Repressor Proteins (genetics), Transcription Factors (antagonists & inhibitors), Transcription Factors (genetics), Transcription Factors (metabolism).
- MESH :
- chemical , antagonists & inhibitors : Histone Chaperones, Transcription Factors.
- chemical , biosynthesis : Chromosomal Proteins, Non-Histone, Repressor Proteins.
- chemical , genetics : Chromatin, Chromosomal Proteins, Non-Histone, DNA-Binding Proteins, Heterochromatin, Histone Chaperones, Repressor Proteins, Transcription Factors.
- drug effects : DNA Breaks, Double-Stranded.
- genetics : DNA Damage, Recombinational DNA Repair.
- chemical , metabolism : Histone Chaperones, Transcription Factors.
- Humans.
Abstract
Cells experience damage from exogenous and endogenous sources that endanger genome stability. Several cellular pathways have evolved to detect DNA damage and mediate its repair. Although many proteins have been implicated in these processes, only recent studies have revealed how they operate in the context of high-ordered chromatin structure. Here, we identify the nuclear oncogene SET (I2PP2A) as a modulator of DNA damage response (DDR) and repair in chromatin surrounding double-strand breaks (DSBs). We demonstrate that depletion of SET increases DDR and survival in the presence of radiomimetic drugs, while overexpression of SET impairs DDR and homologous recombination (HR)-mediated DNA repair. SET interacts with the Kruppel-associated box (KRAB)-associated co-repressor KAP1, and its overexpression results in the sustained retention of KAP1 and Heterochromatin protein 1 (HP1) on chromatin. Our results are consistent with a model in which SET-mediated chromatin compaction triggers an inhibition of DNA end resection and HR.
DOI: 10.1016/j.celrep.2015.03.005
PubMed: 25818296
Affiliations:
- Australie, Canada, France, Grèce
- Alsace (région administrative), Attique (région), Grand Est
- Athènes, Strasbourg
Links toward previous steps (curation, corpus...)
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Le document en format XML
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<country xml:lang="fr">Canada</country>
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<author><name sortKey="Brino, Laurent" sort="Brino, Laurent" uniqKey="Brino L" first="Laurent" last="Brino">Laurent Brino</name>
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<country xml:lang="fr">France</country>
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<country xml:lang="fr">Canada</country>
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<author><name sortKey="Gorgoulis, Vassilis G" sort="Gorgoulis, Vassilis G" uniqKey="Gorgoulis V" first="Vassilis G" last="Gorgoulis">Vassilis G. Gorgoulis</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Chromatin (genetics)</term>
<term>Chromosomal Proteins, Non-Histone (biosynthesis)</term>
<term>Chromosomal Proteins, Non-Histone (genetics)</term>
<term>DNA Breaks, Double-Stranded (drug effects)</term>
<term>DNA Damage (genetics)</term>
<term>DNA-Binding Proteins (genetics)</term>
<term>Heterochromatin (genetics)</term>
<term>Histone Chaperones (antagonists & inhibitors)</term>
<term>Histone Chaperones (genetics)</term>
<term>Histone Chaperones (metabolism)</term>
<term>Humans</term>
<term>Recombinational DNA Repair (genetics)</term>
<term>Repressor Proteins (biosynthesis)</term>
<term>Repressor Proteins (genetics)</term>
<term>Transcription Factors (antagonists & inhibitors)</term>
<term>Transcription Factors (genetics)</term>
<term>Transcription Factors (metabolism)</term>
</keywords>
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<term>Cassures double-brin de l'ADN ()</term>
<term>Chaperons d'histones (antagonistes et inhibiteurs)</term>
<term>Chaperons d'histones (génétique)</term>
<term>Chaperons d'histones (métabolisme)</term>
<term>Chromatine (génétique)</term>
<term>Facteurs de transcription (antagonistes et inhibiteurs)</term>
<term>Facteurs de transcription (génétique)</term>
<term>Facteurs de transcription (métabolisme)</term>
<term>Humains</term>
<term>Hétérochromatine (génétique)</term>
<term>Protéines chromosomiques nonhistones (biosynthèse)</term>
<term>Protéines chromosomiques nonhistones (génétique)</term>
<term>Protéines de liaison à l'ADN (génétique)</term>
<term>Protéines de répression (biosynthèse)</term>
<term>Protéines de répression (génétique)</term>
<term>Réparation de l'ADN par recombinaison (génétique)</term>
</keywords>
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<term>Transcription Factors</term>
</keywords>
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<term>Repressor Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Chromatin</term>
<term>Chromosomal Proteins, Non-Histone</term>
<term>DNA-Binding Proteins</term>
<term>Heterochromatin</term>
<term>Histone Chaperones</term>
<term>Repressor Proteins</term>
<term>Transcription Factors</term>
</keywords>
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<term>Facteurs de transcription</term>
</keywords>
<keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Protéines chromosomiques nonhistones</term>
<term>Protéines de répression</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>DNA Breaks, Double-Stranded</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>DNA Damage</term>
<term>Recombinational DNA Repair</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Altération de l'ADN</term>
<term>Chaperons d'histones</term>
<term>Chromatine</term>
<term>Facteurs de transcription</term>
<term>Hétérochromatine</term>
<term>Protéines chromosomiques nonhistones</term>
<term>Protéines de liaison à l'ADN</term>
<term>Protéines de répression</term>
<term>Réparation de l'ADN par recombinaison</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Histone Chaperones</term>
<term>Transcription Factors</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Chaperons d'histones</term>
<term>Facteurs de transcription</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Humans</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Cassures double-brin de l'ADN</term>
<term>Humains</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Cells experience damage from exogenous and endogenous sources that endanger genome stability. Several cellular pathways have evolved to detect DNA damage and mediate its repair. Although many proteins have been implicated in these processes, only recent studies have revealed how they operate in the context of high-ordered chromatin structure. Here, we identify the nuclear oncogene SET (I2PP2A) as a modulator of DNA damage response (DDR) and repair in chromatin surrounding double-strand breaks (DSBs). We demonstrate that depletion of SET increases DDR and survival in the presence of radiomimetic drugs, while overexpression of SET impairs DDR and homologous recombination (HR)-mediated DNA repair. SET interacts with the Kruppel-associated box (KRAB)-associated co-repressor KAP1, and its overexpression results in the sustained retention of KAP1 and Heterochromatin protein 1 (HP1) on chromatin. Our results are consistent with a model in which SET-mediated chromatin compaction triggers an inhibition of DNA end resection and HR.</div>
</front>
</TEI>
<affiliations><list><country><li>Australie</li>
<li>Canada</li>
<li>France</li>
<li>Grèce</li>
</country>
<region><li>Alsace (région administrative)</li>
<li>Attique (région)</li>
<li>Grand Est</li>
</region>
<settlement><li>Athènes</li>
<li>Strasbourg</li>
</settlement>
</list>
<tree><country name="France"><region name="Grand Est"><name sortKey="Kalousi, Alkmini" sort="Kalousi, Alkmini" uniqKey="Kalousi A" first="Alkmini" last="Kalousi">Alkmini Kalousi</name>
</region>
<name sortKey="Brino, Laurent" sort="Brino, Laurent" uniqKey="Brino L" first="Laurent" last="Brino">Laurent Brino</name>
<name sortKey="Hoffbeck, Anne Sophie" sort="Hoffbeck, Anne Sophie" uniqKey="Hoffbeck A" first="Anne-Sophie" last="Hoffbeck">Anne-Sophie Hoffbeck</name>
<name sortKey="Soutoglou, Evi" sort="Soutoglou, Evi" uniqKey="Soutoglou E" first="Evi" last="Soutoglou">Evi Soutoglou</name>
</country>
<country name="Grèce"><region name="Attique (région)"><name sortKey="Selemenakis, Platonas N" sort="Selemenakis, Platonas N" uniqKey="Selemenakis P" first="Platonas N" last="Selemenakis">Platonas N. Selemenakis</name>
</region>
<name sortKey="Gorgoulis, Vassilis G" sort="Gorgoulis, Vassilis G" uniqKey="Gorgoulis V" first="Vassilis G" last="Gorgoulis">Vassilis G. Gorgoulis</name>
</country>
<country name="Canada"><noRegion><name sortKey="Pinder, Jordan" sort="Pinder, Jordan" uniqKey="Pinder J" first="Jordan" last="Pinder">Jordan Pinder</name>
</noRegion>
<name sortKey="Dellaire, Graham" sort="Dellaire, Graham" uniqKey="Dellaire G" first="Graham" last="Dellaire">Graham Dellaire</name>
</country>
<country name="Australie"><noRegion><name sortKey="Savage, Kienan I" sort="Savage, Kienan I" uniqKey="Savage K" first="Kienan I" last="Savage">Kienan I. Savage</name>
</noRegion>
<name sortKey="Khanna, Kum Kum" sort="Khanna, Kum Kum" uniqKey="Khanna K" first="Kum Kum" last="Khanna">Kum Kum Khanna</name>
</country>
</tree>
</affiliations>
</record>
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