DR5 related autophagy can promote apoptosis in gliomas after irradiation.
Identifieur interne : 000130 ( Main/Exploration ); précédent : 000129; suivant : 000131DR5 related autophagy can promote apoptosis in gliomas after irradiation.
Auteurs : Peng Zhang [République populaire de Chine] ; Hailong Wang [République populaire de Chine] ; Yu Chen [République populaire de Chine] ; Adil Farooq Lodhi [Pakistan] ; Chunli Sun [République populaire de Chine] ; Feiyi Sun [République populaire de Chine] ; Liben Yan [République populaire de Chine] ; Yulin Deng [République populaire de Chine] ; Hong Ma [République populaire de Chine]Source :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2020.
Descripteurs français
- KwdFr :
- Apoptose (effets des radiations), Apoptose (génétique), Autophagie (effets des radiations), Autophagie (génétique), Caspase 8 (métabolisme), Gliome (anatomopathologie), Gliome (génétique), Gliome (radiothérapie), Histone (métabolisme), Humains (MeSH), Lignée cellulaire tumorale (MeSH), Méthylation (MeSH), Récepteurs de TRAIL (génétique), Récepteurs de TRAIL (métabolisme), Régulation de l'expression des gènes tumoraux (MeSH), Transcription génétique (MeSH), Tumeurs du cerveau (anatomopathologie), Tumeurs du cerveau (génétique), Tumeurs du cerveau (radiothérapie).
- MESH :
- anatomopathologie : Gliome, Tumeurs du cerveau.
- effets des radiations : Apoptose, Autophagie.
- génétique : Apoptose, Autophagie, Gliome, Récepteurs de TRAIL, Tumeurs du cerveau.
- métabolisme : Caspase 8, Histone, Récepteurs de TRAIL.
- radiothérapie : Gliome, Tumeurs du cerveau.
- Humains, Lignée cellulaire tumorale, Méthylation, Régulation de l'expression des gènes tumoraux, Transcription génétique.
English descriptors
- KwdEn :
- Apoptosis (genetics), Apoptosis (radiation effects), Autophagy (genetics), Autophagy (radiation effects), Brain Neoplasms (genetics), Brain Neoplasms (pathology), Brain Neoplasms (radiotherapy), Caspase 8 (metabolism), Cell Line, Tumor (MeSH), Gene Expression Regulation, Neoplastic (MeSH), Glioma (genetics), Glioma (pathology), Glioma (radiotherapy), Histones (metabolism), Humans (MeSH), Methylation (MeSH), Receptors, TNF-Related Apoptosis-Inducing Ligand (genetics), Receptors, TNF-Related Apoptosis-Inducing Ligand (metabolism), Transcription, Genetic (MeSH).
- MESH :
- chemical , genetics : Receptors, TNF-Related Apoptosis-Inducing Ligand.
- chemical , metabolism : Caspase 8, Histones, Receptors, TNF-Related Apoptosis-Inducing Ligand.
- genetics : Apoptosis, Autophagy, Brain Neoplasms, Glioma.
- pathology : Brain Neoplasms, Glioma.
- radiation effects : Apoptosis, Autophagy.
- radiotherapy : Brain Neoplasms, Glioma.
- Cell Line, Tumor, Gene Expression Regulation, Neoplastic, Humans, Methylation, Transcription, Genetic.
Abstract
As a cancer treatment strategy, irradiation therapy is widely used that can cause DNA breakage and increase free radicals, which leads to different types of cell death. Among them, apoptosis and autophagy are the most important and the most studied cell death processes. Although the exploration of the relationship between apoptosis and autophagy has been a major area of focus, still the molecular mechanisms of autophagy on apoptosis remain unclear. Here, we have revealed that apoptosis was enhanced by the death receptor 5 (DR5) pathway, and the effect of autophagy on apoptosis was promoted by DR5 interacting with LC3B as well as Caspase8 in gliomas after irradiation. Interestingly, we observed that the addition of four different autophagy inducers, rapamycin (RAP), CCI779, ABT737 and temozolomide (TMZ), induced the differences of DR5 expression and cell apoptosis after irradiation. Unlike RAP and CCI779, ABT737 and TMZ were able to increase DR5 expression and further induce cell death. Therefore, we have concluded that DR5 plays a novel and indispensable role in promoting cell apoptosis under irradiation and suggest a potential therapeutic approach for glioblastoma treatment.
DOI: 10.1016/j.bbrc.2019.11.161
PubMed: 31806377
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Electronic address: 04656@bit.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Life Science, Beijing Institute of Technology, Beijing, 100081</wicri:regionArea><wicri:noRegion>100081</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:31806377</idno><idno type="pmid">31806377</idno><idno type="doi">10.1016/j.bbrc.2019.11.161</idno><idno type="wicri:Area/Main/Corpus">000149</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000149</idno><idno type="wicri:Area/Main/Curation">000149</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000149</idno><idno type="wicri:Area/Main/Exploration">000149</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">DR5 related autophagy can promote apoptosis in gliomas after irradiation.</title><author><name sortKey="Zhang, Peng" sort="Zhang, Peng" uniqKey="Zhang P" first="Peng" last="Zhang">Peng Zhang</name><affiliation wicri:level="1"><nlm:affiliation>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Life Science, Beijing Institute of Technology, Beijing, 100081</wicri:regionArea><wicri:noRegion>100081</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Hailong" sort="Wang, Hailong" uniqKey="Wang H" first="Hailong" last="Wang">Hailong Wang</name><affiliation wicri:level="1"><nlm:affiliation>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Life Science, Beijing Institute of Technology, Beijing, 100081</wicri:regionArea><wicri:noRegion>100081</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Yu" sort="Chen, Yu" uniqKey="Chen Y" first="Yu" last="Chen">Yu Chen</name><affiliation wicri:level="1"><nlm:affiliation>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Life Science, Beijing Institute of Technology, Beijing, 100081</wicri:regionArea><wicri:noRegion>100081</wicri:noRegion></affiliation></author><author><name sortKey="Lodhi, Adil Farooq" sort="Lodhi, Adil Farooq" uniqKey="Lodhi A" first="Adil Farooq" last="Lodhi">Adil Farooq Lodhi</name><affiliation wicri:level="1"><nlm:affiliation>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China; Department of Microbiology, Faculty of Health Sciences, Hazara University, Mansehra, Pakistan.</nlm:affiliation><country xml:lang="fr">Pakistan</country><wicri:regionArea>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China; Department of Microbiology, Faculty of Health Sciences, Hazara University, Mansehra</wicri:regionArea><wicri:noRegion>Mansehra</wicri:noRegion></affiliation></author><author><name sortKey="Sun, Chunli" sort="Sun, Chunli" uniqKey="Sun C" first="Chunli" last="Sun">Chunli Sun</name><affiliation wicri:level="1"><nlm:affiliation>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Life Science, Beijing Institute of Technology, Beijing, 100081</wicri:regionArea><wicri:noRegion>100081</wicri:noRegion></affiliation></author><author><name sortKey="Sun, Feiyi" sort="Sun, Feiyi" uniqKey="Sun F" first="Feiyi" last="Sun">Feiyi Sun</name><affiliation wicri:level="1"><nlm:affiliation>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Life Science, Beijing Institute of Technology, Beijing, 100081</wicri:regionArea><wicri:noRegion>100081</wicri:noRegion></affiliation></author><author><name sortKey="Yan, Liben" sort="Yan, Liben" uniqKey="Yan L" first="Liben" last="Yan">Liben Yan</name><affiliation wicri:level="1"><nlm:affiliation>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Life Science, Beijing Institute of Technology, Beijing, 100081</wicri:regionArea><wicri:noRegion>100081</wicri:noRegion></affiliation></author><author><name sortKey="Deng, Yulin" sort="Deng, Yulin" uniqKey="Deng Y" first="Yulin" last="Deng">Yulin Deng</name><affiliation wicri:level="1"><nlm:affiliation>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Life Science, Beijing Institute of Technology, Beijing, 100081</wicri:regionArea><wicri:noRegion>100081</wicri:noRegion></affiliation></author><author><name sortKey="Ma, Hong" sort="Ma, Hong" uniqKey="Ma H" first="Hong" last="Ma">Hong Ma</name><affiliation wicri:level="1"><nlm:affiliation>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China. Electronic address: 04656@bit.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Life Science, Beijing Institute of Technology, Beijing, 100081</wicri:regionArea><wicri:noRegion>100081</wicri:noRegion></affiliation></author></analytic><series><title level="j">Biochemical and biophysical research communications</title><idno type="eISSN">1090-2104</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis (genetics)</term><term>Apoptosis (radiation effects)</term><term>Autophagy (genetics)</term><term>Autophagy (radiation effects)</term><term>Brain Neoplasms (genetics)</term><term>Brain Neoplasms (pathology)</term><term>Brain Neoplasms (radiotherapy)</term><term>Caspase 8 (metabolism)</term><term>Cell Line, Tumor (MeSH)</term><term>Gene Expression Regulation, Neoplastic (MeSH)</term><term>Glioma (genetics)</term><term>Glioma (pathology)</term><term>Glioma (radiotherapy)</term><term>Histones (metabolism)</term><term>Humans (MeSH)</term><term>Methylation (MeSH)</term><term>Receptors, TNF-Related Apoptosis-Inducing Ligand (genetics)</term><term>Receptors, TNF-Related Apoptosis-Inducing Ligand (metabolism)</term><term>Transcription, Genetic (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Apoptose (effets des radiations)</term><term>Apoptose (génétique)</term><term>Autophagie (effets des radiations)</term><term>Autophagie (génétique)</term><term>Caspase 8 (métabolisme)</term><term>Gliome (anatomopathologie)</term><term>Gliome (génétique)</term><term>Gliome (radiothérapie)</term><term>Histone (métabolisme)</term><term>Humains (MeSH)</term><term>Lignée cellulaire tumorale (MeSH)</term><term>Méthylation (MeSH)</term><term>Récepteurs de TRAIL (génétique)</term><term>Récepteurs de TRAIL (métabolisme)</term><term>Régulation de l'expression des gènes tumoraux (MeSH)</term><term>Transcription génétique (MeSH)</term><term>Tumeurs du cerveau (anatomopathologie)</term><term>Tumeurs du cerveau (génétique)</term><term>Tumeurs du cerveau (radiothérapie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Receptors, TNF-Related Apoptosis-Inducing Ligand</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Caspase 8</term><term>Histones</term><term>Receptors, TNF-Related Apoptosis-Inducing Ligand</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Gliome</term><term>Tumeurs du cerveau</term></keywords><keywords scheme="MESH" qualifier="effets des radiations" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Brain Neoplasms</term><term>Glioma</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term><term>Gliome</term><term>Récepteurs de TRAIL</term><term>Tumeurs du cerveau</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Caspase 8</term><term>Histone</term><term>Récepteurs de TRAIL</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain Neoplasms</term><term>Glioma</term></keywords><keywords scheme="MESH" qualifier="radiation effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term></keywords><keywords scheme="MESH" qualifier="radiotherapy" xml:lang="en"><term>Brain Neoplasms</term><term>Glioma</term></keywords><keywords scheme="MESH" qualifier="radiothérapie" xml:lang="fr"><term>Gliome</term><term>Tumeurs du cerveau</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Gene Expression Regulation, Neoplastic</term><term>Humans</term><term>Methylation</term><term>Transcription, Genetic</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Méthylation</term><term>Régulation de l'expression des gènes tumoraux</term><term>Transcription génétique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">As a cancer treatment strategy, irradiation therapy is widely used that can cause DNA breakage and increase free radicals, which leads to different types of cell death. Among them, apoptosis and autophagy are the most important and the most studied cell death processes. Although the exploration of the relationship between apoptosis and autophagy has been a major area of focus, still the molecular mechanisms of autophagy on apoptosis remain unclear. Here, we have revealed that apoptosis was enhanced by the death receptor 5 (DR5) pathway, and the effect of autophagy on apoptosis was promoted by DR5 interacting with LC3B as well as Caspase8 in gliomas after irradiation. Interestingly, we observed that the addition of four different autophagy inducers, rapamycin (RAP), CCI779, ABT737 and temozolomide (TMZ), induced the differences of DR5 expression and cell apoptosis after irradiation. Unlike RAP and CCI779, ABT737 and TMZ were able to increase DR5 expression and further induce cell death. Therefore, we have concluded that DR5 plays a novel and indispensable role in promoting cell apoptosis under irradiation and suggest a potential therapeutic approach for glioblastoma treatment.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31806377</PMID><DateCompleted><Year>2020</Year><Month>08</Month><Day>31</Day></DateCompleted><DateRevised><Year>2020</Year><Month>08</Month><Day>31</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2104</ISSN><JournalIssue CitedMedium="Internet"><Volume>522</Volume><Issue>4</Issue><PubDate><Year>2020</Year><Month>02</Month><Day>19</Day></PubDate></JournalIssue><Title>Biochemical and biophysical research communications</Title><ISOAbbreviation>Biochem Biophys Res Commun</ISOAbbreviation></Journal><ArticleTitle>DR5 related autophagy can promote apoptosis in gliomas after irradiation.</ArticleTitle><Pagination><MedlinePgn>910-916</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0006-291X(19)32289-2</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbrc.2019.11.161</ELocationID><Abstract><AbstractText>As a cancer treatment strategy, irradiation therapy is widely used that can cause DNA breakage and increase free radicals, which leads to different types of cell death. Among them, apoptosis and autophagy are the most important and the most studied cell death processes. Although the exploration of the relationship between apoptosis and autophagy has been a major area of focus, still the molecular mechanisms of autophagy on apoptosis remain unclear. Here, we have revealed that apoptosis was enhanced by the death receptor 5 (DR5) pathway, and the effect of autophagy on apoptosis was promoted by DR5 interacting with LC3B as well as Caspase8 in gliomas after irradiation. Interestingly, we observed that the addition of four different autophagy inducers, rapamycin (RAP), CCI779, ABT737 and temozolomide (TMZ), induced the differences of DR5 expression and cell apoptosis after irradiation. Unlike RAP and CCI779, ABT737 and TMZ were able to increase DR5 expression and further induce cell death. Therefore, we have concluded that DR5 plays a novel and indispensable role in promoting cell apoptosis under irradiation and suggest a potential therapeutic approach for glioblastoma treatment.</AbstractText><CopyrightInformation>Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Peng</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Hailong</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Yu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lodhi</LastName><ForeName>Adil Farooq</ForeName><Initials>AF</Initials><AffiliationInfo><Affiliation>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China; Department of Microbiology, Faculty of Health Sciences, Hazara University, Mansehra, Pakistan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Chunli</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Feiyi</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yan</LastName><ForeName>Liben</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Deng</LastName><ForeName>Yulin</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Hong</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>School of Life Science, Beijing Institute of Technology, Beijing, 100081, China. Electronic address: 04656@bit.edu.cn.</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></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>12</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Biochem Biophys Res Commun</MedlineTA><NlmUniqueID>0372516</NlmUniqueID><ISSNLinking>0006-291X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006657">Histones</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053220">Receptors, TNF-Related Apoptosis-Inducing Ligand</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C505639">TNFRSF10B protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="D053181">Caspase 8</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="Y">Apoptosis</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000528" MajorTopicYN="N">radiation effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="Y">Autophagy</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000528" MajorTopicYN="N">radiation effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001932" MajorTopicYN="N">Brain Neoplasms</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName><QualifierName UI="Q000532" MajorTopicYN="Y">radiotherapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053181" MajorTopicYN="N">Caspase 8</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015972" MajorTopicYN="N">Gene Expression Regulation, Neoplastic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005910" MajorTopicYN="N">Glioma</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName><QualifierName UI="Q000532" MajorTopicYN="Y">radiotherapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006657" MajorTopicYN="N">Histones</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008745" MajorTopicYN="N">Methylation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053220" MajorTopicYN="N">Receptors, TNF-Related Apoptosis-Inducing Ligand</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014158" MajorTopicYN="N">Transcription, Genetic</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Apoptosis</Keyword><Keyword MajorTopicYN="Y">Autophagy</Keyword><Keyword MajorTopicYN="Y">DR5</Keyword><Keyword MajorTopicYN="Y">Glioma</Keyword><Keyword MajorTopicYN="Y">Irradiation tolerance</Keyword></KeywordList><CoiStatement>Declaration of competing interest None.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>11</Month><Day>08</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>11</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>12</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>9</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>12</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31806377</ArticleId><ArticleId IdType="pii">S0006-291X(19)32289-2</ArticleId><ArticleId IdType="doi">10.1016/j.bbrc.2019.11.161</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Pakistan</li><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Zhang, Peng" sort="Zhang, Peng" uniqKey="Zhang P" first="Peng" last="Zhang">Peng Zhang</name></noRegion><name sortKey="Chen, Yu" sort="Chen, Yu" uniqKey="Chen Y" first="Yu" last="Chen">Yu Chen</name><name sortKey="Deng, Yulin" sort="Deng, Yulin" uniqKey="Deng Y" first="Yulin" last="Deng">Yulin Deng</name><name sortKey="Ma, Hong" sort="Ma, Hong" uniqKey="Ma H" first="Hong" last="Ma">Hong Ma</name><name sortKey="Sun, Chunli" sort="Sun, Chunli" uniqKey="Sun C" first="Chunli" last="Sun">Chunli Sun</name><name sortKey="Sun, Feiyi" sort="Sun, Feiyi" uniqKey="Sun F" first="Feiyi" last="Sun">Feiyi Sun</name><name sortKey="Wang, Hailong" sort="Wang, Hailong" uniqKey="Wang H" first="Hailong" last="Wang">Hailong Wang</name><name sortKey="Yan, Liben" sort="Yan, Liben" uniqKey="Yan L" first="Liben" last="Yan">Liben Yan</name></country><country name="Pakistan"><noRegion><name sortKey="Lodhi, Adil Farooq" sort="Lodhi, Adil Farooq" uniqKey="Lodhi A" first="Adil Farooq" last="Lodhi">Adil Farooq Lodhi</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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