EBV infection is associated with histone bivalent switch modifications in squamous epithelial cells
Epstein−Barr virus (EBV) induces histone modifications to regulate signaling pathways involved in EBV-driven tumorigenesis. To date, the regulatory mechanisms involved are poorly understood. In this study, we show that EBV infection of epithelial cells is associated with aberrant histone modificatio...
Gespeichert in:
| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2019-07, Vol.116 (28), p.14144-14153 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 14153 |
|---|---|
| container_issue | 28 |
| container_start_page | 14144 |
| container_title | Proceedings of the National Academy of Sciences - PNAS |
| container_volume | 116 |
| creator | Leong, Merrin Man Long Cheung, Arthur Kwok Leung Dai, Wei Tsao, Sai Wah Tsang, Chi Man Dawson, Christopher W. Ko, Josephine Mun Yee Lung, Maria Li |
| description | Epstein−Barr virus (EBV) induces histone modifications to regulate signaling pathways involved in EBV-driven tumorigenesis. To date, the regulatory mechanisms involved are poorly understood. In this study, we show that EBV infection of epithelial cells is associated with aberrant histone modification; specifically, aberrant histone bivalent switches by reducing the transcriptional activation histone mark (H3K4me3) and enhancing the suppressive mark (H3K27me3) at the promoter regions of a panel of DNA damage repair members in immortalized nasopharyngeal epithelial (NPE) cells. Sixteen DNA damage repair family members in base excision repair (BER), homologous recombination, nonhomologous end-joining, and mismatch repair (MMR) pathways showed aberrant histone bivalent switches. Among this panel of DNA repair members, MLH1, involved in MMR, was significantly down-regulated in EBV-infected NPE cells through aberrant histone bivalent switches in a promoter hypermethylation-independent manner. Functionally, expression of MLH1 correlated closely with cisplatin sensitivity both in vitro and in vivo. Moreover, seven BER members with aberrant histone bivalent switches in the EBV-positive NPE cell lines were significantly enriched in pathway analysis in a promoter hypermethylation-independent manner. This observation is further validated by their down-regulation in EBV-infected NPE cells. The in vitro comet and apurinic/apyrimidinic site assays further confirmed that EBV-infected NPE cells showed reduced DNA damage repair responsiveness. These findings suggest the importance of EBV-associated aberrant histone bivalent switch in host cells in subsequent suppression of DNA damage repair genes in a methylation-independent manner. |
| doi_str_mv | 10.1073/pnas.1821752116 |
| format | Article |
| fullrecord | <record><control><sourceid>jstor_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6628793</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><jstor_id>26760998</jstor_id><sourcerecordid>26760998</sourcerecordid><originalsourceid>FETCH-LOGICAL-c443t-a4e67b07dca2a7f29aa028826526cd1b7e0c9b0390e16d03517cededb52c9f293</originalsourceid><addsrcrecordid>eNpdkc1r3DAQxUVJaTabnnNqEeTSi5ORZOvjEmhD-gGBXJJehSyPu1psa2PZCfnvq2XTTRMQDGh-7zGPR8gJgzMGSpxvBpfOmOZMVZwx-Y4sGBhWyNLAAVkAcFXokpeH5CilNQCYSsMHcigYF1Vl1IL4q2-_aRha9FOIAw2JupSiD27Chj6GaUVXIU1xQFqHB9fhMNGUv_2K9rEJbfBuq0vZgqb72fVxThQ3WYddcB312HXpmLxvXZfw4_NckrvvV7eXP4vrmx-_Lr9eF74sxVS4EqWqQTXecadabpwDrjWXFZe-YbVC8KYGYQCZbEBUTHlssKkr7k3GxZJc7Hw3c91j4_Oxo-vsZgy9G59sdMG-3gxhZf_EBysl18qIbPDl2WCM9zOmyfYhbSO4AXMwy3kpDUhQOqOnb9B1nMchx8uU1FJzkd-SnO8oP8aURmz3xzCw2wLttkD7UmBWfP4_w57_11gGPu2Ada5l3O-5VBKM0eIvJwmjHg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2268682382</pqid></control><display><type>article</type><title>EBV infection is associated with histone bivalent switch modifications in squamous epithelial cells</title><source>Jstor Complete Legacy</source><source>MEDLINE</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><source>Free Full-Text Journals in Chemistry</source><creator>Leong, Merrin Man Long ; Cheung, Arthur Kwok Leung ; Dai, Wei ; Tsao, Sai Wah ; Tsang, Chi Man ; Dawson, Christopher W. ; Ko, Josephine Mun Yee ; Lung, Maria Li</creator><creatorcontrib>Leong, Merrin Man Long ; Cheung, Arthur Kwok Leung ; Dai, Wei ; Tsao, Sai Wah ; Tsang, Chi Man ; Dawson, Christopher W. ; Ko, Josephine Mun Yee ; Lung, Maria Li</creatorcontrib><description>Epstein−Barr virus (EBV) induces histone modifications to regulate signaling pathways involved in EBV-driven tumorigenesis. To date, the regulatory mechanisms involved are poorly understood. In this study, we show that EBV infection of epithelial cells is associated with aberrant histone modification; specifically, aberrant histone bivalent switches by reducing the transcriptional activation histone mark (H3K4me3) and enhancing the suppressive mark (H3K27me3) at the promoter regions of a panel of DNA damage repair members in immortalized nasopharyngeal epithelial (NPE) cells. Sixteen DNA damage repair family members in base excision repair (BER), homologous recombination, nonhomologous end-joining, and mismatch repair (MMR) pathways showed aberrant histone bivalent switches. Among this panel of DNA repair members, MLH1, involved in MMR, was significantly down-regulated in EBV-infected NPE cells through aberrant histone bivalent switches in a promoter hypermethylation-independent manner. Functionally, expression of MLH1 correlated closely with cisplatin sensitivity both in vitro and in vivo. Moreover, seven BER members with aberrant histone bivalent switches in the EBV-positive NPE cell lines were significantly enriched in pathway analysis in a promoter hypermethylation-independent manner. This observation is further validated by their down-regulation in EBV-infected NPE cells. The in vitro comet and apurinic/apyrimidinic site assays further confirmed that EBV-infected NPE cells showed reduced DNA damage repair responsiveness. These findings suggest the importance of EBV-associated aberrant histone bivalent switch in host cells in subsequent suppression of DNA damage repair genes in a methylation-independent manner.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.1821752116</identifier><identifier>PMID: 31235597</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Aberration ; Base excision repair ; Biological Sciences ; Cisplatin ; CpG Islands - genetics ; Damage ; Deoxyribonucleic acid ; DNA ; DNA damage ; DNA Damage - genetics ; DNA methylation ; DNA Methylation - genetics ; DNA Mismatch Repair - genetics ; DNA repair ; DNA Repair - genetics ; Epithelial cells ; Epithelial Cells - metabolism ; Epithelial Cells - virology ; Epstein-Barr virus ; Epstein-Barr Virus Infections - genetics ; Epstein-Barr Virus Infections - pathology ; Epstein-Barr Virus Infections - virology ; Gene Expression Regulation - genetics ; Herpesvirus 4, Human - genetics ; Herpesvirus 4, Human - pathogenicity ; Histone Code - genetics ; Histones ; Histones - genetics ; Homologous recombination ; Homologous Recombination - genetics ; Homology ; Humans ; Mismatch repair ; MLH1 protein ; MutL Protein Homolog 1 - genetics ; Nasopharynx - growth & development ; Nasopharynx - pathology ; Nasopharynx - virology ; PNAS Plus ; Promoter Regions, Genetic ; Regulatory mechanisms (biology) ; Repair ; Switches ; Transcription activation ; Tumorigenesis ; Viruses</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2019-07, Vol.116 (28), p.14144-14153</ispartof><rights>Copyright National Academy of Sciences Jul 9, 2019</rights><rights>2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c443t-a4e67b07dca2a7f29aa028826526cd1b7e0c9b0390e16d03517cededb52c9f293</citedby><cites>FETCH-LOGICAL-c443t-a4e67b07dca2a7f29aa028826526cd1b7e0c9b0390e16d03517cededb52c9f293</cites><orcidid>0000-0003-2559-3626</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/26760998$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/26760998$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,723,776,780,799,881,27901,27902,53766,53768,57992,58225</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31235597$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Leong, Merrin Man Long</creatorcontrib><creatorcontrib>Cheung, Arthur Kwok Leung</creatorcontrib><creatorcontrib>Dai, Wei</creatorcontrib><creatorcontrib>Tsao, Sai Wah</creatorcontrib><creatorcontrib>Tsang, Chi Man</creatorcontrib><creatorcontrib>Dawson, Christopher W.</creatorcontrib><creatorcontrib>Ko, Josephine Mun Yee</creatorcontrib><creatorcontrib>Lung, Maria Li</creatorcontrib><title>EBV infection is associated with histone bivalent switch modifications in squamous epithelial cells</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Epstein−Barr virus (EBV) induces histone modifications to regulate signaling pathways involved in EBV-driven tumorigenesis. To date, the regulatory mechanisms involved are poorly understood. In this study, we show that EBV infection of epithelial cells is associated with aberrant histone modification; specifically, aberrant histone bivalent switches by reducing the transcriptional activation histone mark (H3K4me3) and enhancing the suppressive mark (H3K27me3) at the promoter regions of a panel of DNA damage repair members in immortalized nasopharyngeal epithelial (NPE) cells. Sixteen DNA damage repair family members in base excision repair (BER), homologous recombination, nonhomologous end-joining, and mismatch repair (MMR) pathways showed aberrant histone bivalent switches. Among this panel of DNA repair members, MLH1, involved in MMR, was significantly down-regulated in EBV-infected NPE cells through aberrant histone bivalent switches in a promoter hypermethylation-independent manner. Functionally, expression of MLH1 correlated closely with cisplatin sensitivity both in vitro and in vivo. Moreover, seven BER members with aberrant histone bivalent switches in the EBV-positive NPE cell lines were significantly enriched in pathway analysis in a promoter hypermethylation-independent manner. This observation is further validated by their down-regulation in EBV-infected NPE cells. The in vitro comet and apurinic/apyrimidinic site assays further confirmed that EBV-infected NPE cells showed reduced DNA damage repair responsiveness. These findings suggest the importance of EBV-associated aberrant histone bivalent switch in host cells in subsequent suppression of DNA damage repair genes in a methylation-independent manner.</description><subject>Aberration</subject><subject>Base excision repair</subject><subject>Biological Sciences</subject><subject>Cisplatin</subject><subject>CpG Islands - genetics</subject><subject>Damage</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA damage</subject><subject>DNA Damage - genetics</subject><subject>DNA methylation</subject><subject>DNA Methylation - genetics</subject><subject>DNA Mismatch Repair - genetics</subject><subject>DNA repair</subject><subject>DNA Repair - genetics</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial Cells - virology</subject><subject>Epstein-Barr virus</subject><subject>Epstein-Barr Virus Infections - genetics</subject><subject>Epstein-Barr Virus Infections - pathology</subject><subject>Epstein-Barr Virus Infections - virology</subject><subject>Gene Expression Regulation - genetics</subject><subject>Herpesvirus 4, Human - genetics</subject><subject>Herpesvirus 4, Human - pathogenicity</subject><subject>Histone Code - genetics</subject><subject>Histones</subject><subject>Histones - genetics</subject><subject>Homologous recombination</subject><subject>Homologous Recombination - genetics</subject><subject>Homology</subject><subject>Humans</subject><subject>Mismatch repair</subject><subject>MLH1 protein</subject><subject>MutL Protein Homolog 1 - genetics</subject><subject>Nasopharynx - growth & development</subject><subject>Nasopharynx - pathology</subject><subject>Nasopharynx - virology</subject><subject>PNAS Plus</subject><subject>Promoter Regions, Genetic</subject><subject>Regulatory mechanisms (biology)</subject><subject>Repair</subject><subject>Switches</subject><subject>Transcription activation</subject><subject>Tumorigenesis</subject><subject>Viruses</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc1r3DAQxUVJaTabnnNqEeTSi5ORZOvjEmhD-gGBXJJehSyPu1psa2PZCfnvq2XTTRMQDGh-7zGPR8gJgzMGSpxvBpfOmOZMVZwx-Y4sGBhWyNLAAVkAcFXokpeH5CilNQCYSsMHcigYF1Vl1IL4q2-_aRha9FOIAw2JupSiD27Chj6GaUVXIU1xQFqHB9fhMNGUv_2K9rEJbfBuq0vZgqb72fVxThQ3WYddcB312HXpmLxvXZfw4_NckrvvV7eXP4vrmx-_Lr9eF74sxVS4EqWqQTXecadabpwDrjWXFZe-YbVC8KYGYQCZbEBUTHlssKkr7k3GxZJc7Hw3c91j4_Oxo-vsZgy9G59sdMG-3gxhZf_EBysl18qIbPDl2WCM9zOmyfYhbSO4AXMwy3kpDUhQOqOnb9B1nMchx8uU1FJzkd-SnO8oP8aURmz3xzCw2wLttkD7UmBWfP4_w57_11gGPu2Ada5l3O-5VBKM0eIvJwmjHg</recordid><startdate>20190709</startdate><enddate>20190709</enddate><creator>Leong, Merrin Man Long</creator><creator>Cheung, Arthur Kwok Leung</creator><creator>Dai, Wei</creator><creator>Tsao, Sai Wah</creator><creator>Tsang, Chi Man</creator><creator>Dawson, Christopher W.</creator><creator>Ko, Josephine Mun Yee</creator><creator>Lung, Maria Li</creator><general>National Academy of Sciences</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-2559-3626</orcidid></search><sort><creationdate>20190709</creationdate><title>EBV infection is associated with histone bivalent switch modifications in squamous epithelial cells</title><author>Leong, Merrin Man Long ; Cheung, Arthur Kwok Leung ; Dai, Wei ; Tsao, Sai Wah ; Tsang, Chi Man ; Dawson, Christopher W. ; Ko, Josephine Mun Yee ; Lung, Maria Li</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c443t-a4e67b07dca2a7f29aa028826526cd1b7e0c9b0390e16d03517cededb52c9f293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Aberration</topic><topic>Base excision repair</topic><topic>Biological Sciences</topic><topic>Cisplatin</topic><topic>CpG Islands - genetics</topic><topic>Damage</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA damage</topic><topic>DNA Damage - genetics</topic><topic>DNA methylation</topic><topic>DNA Methylation - genetics</topic><topic>DNA Mismatch Repair - genetics</topic><topic>DNA repair</topic><topic>DNA Repair - genetics</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - metabolism</topic><topic>Epithelial Cells - virology</topic><topic>Epstein-Barr virus</topic><topic>Epstein-Barr Virus Infections - genetics</topic><topic>Epstein-Barr Virus Infections - pathology</topic><topic>Epstein-Barr Virus Infections - virology</topic><topic>Gene Expression Regulation - genetics</topic><topic>Herpesvirus 4, Human - genetics</topic><topic>Herpesvirus 4, Human - pathogenicity</topic><topic>Histone Code - genetics</topic><topic>Histones</topic><topic>Histones - genetics</topic><topic>Homologous recombination</topic><topic>Homologous Recombination - genetics</topic><topic>Homology</topic><topic>Humans</topic><topic>Mismatch repair</topic><topic>MLH1 protein</topic><topic>MutL Protein Homolog 1 - genetics</topic><topic>Nasopharynx - growth & development</topic><topic>Nasopharynx - pathology</topic><topic>Nasopharynx - virology</topic><topic>PNAS Plus</topic><topic>Promoter Regions, Genetic</topic><topic>Regulatory mechanisms (biology)</topic><topic>Repair</topic><topic>Switches</topic><topic>Transcription activation</topic><topic>Tumorigenesis</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Leong, Merrin Man Long</creatorcontrib><creatorcontrib>Cheung, Arthur Kwok Leung</creatorcontrib><creatorcontrib>Dai, Wei</creatorcontrib><creatorcontrib>Tsao, Sai Wah</creatorcontrib><creatorcontrib>Tsang, Chi Man</creatorcontrib><creatorcontrib>Dawson, Christopher W.</creatorcontrib><creatorcontrib>Ko, Josephine Mun Yee</creatorcontrib><creatorcontrib>Lung, Maria Li</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Leong, Merrin Man Long</au><au>Cheung, Arthur Kwok Leung</au><au>Dai, Wei</au><au>Tsao, Sai Wah</au><au>Tsang, Chi Man</au><au>Dawson, Christopher W.</au><au>Ko, Josephine Mun Yee</au><au>Lung, Maria Li</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>EBV infection is associated with histone bivalent switch modifications in squamous epithelial cells</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2019-07-09</date><risdate>2019</risdate><volume>116</volume><issue>28</issue><spage>14144</spage><epage>14153</epage><pages>14144-14153</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>Epstein−Barr virus (EBV) induces histone modifications to regulate signaling pathways involved in EBV-driven tumorigenesis. To date, the regulatory mechanisms involved are poorly understood. In this study, we show that EBV infection of epithelial cells is associated with aberrant histone modification; specifically, aberrant histone bivalent switches by reducing the transcriptional activation histone mark (H3K4me3) and enhancing the suppressive mark (H3K27me3) at the promoter regions of a panel of DNA damage repair members in immortalized nasopharyngeal epithelial (NPE) cells. Sixteen DNA damage repair family members in base excision repair (BER), homologous recombination, nonhomologous end-joining, and mismatch repair (MMR) pathways showed aberrant histone bivalent switches. Among this panel of DNA repair members, MLH1, involved in MMR, was significantly down-regulated in EBV-infected NPE cells through aberrant histone bivalent switches in a promoter hypermethylation-independent manner. Functionally, expression of MLH1 correlated closely with cisplatin sensitivity both in vitro and in vivo. Moreover, seven BER members with aberrant histone bivalent switches in the EBV-positive NPE cell lines were significantly enriched in pathway analysis in a promoter hypermethylation-independent manner. This observation is further validated by their down-regulation in EBV-infected NPE cells. The in vitro comet and apurinic/apyrimidinic site assays further confirmed that EBV-infected NPE cells showed reduced DNA damage repair responsiveness. These findings suggest the importance of EBV-associated aberrant histone bivalent switch in host cells in subsequent suppression of DNA damage repair genes in a methylation-independent manner.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>31235597</pmid><doi>10.1073/pnas.1821752116</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0003-2559-3626</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0027-8424 |
| ispartof | Proceedings of the National Academy of Sciences - PNAS, 2019-07, Vol.116 (28), p.14144-14153 |
| issn | 0027-8424 1091-6490 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6628793 |
| source | Jstor Complete Legacy; MEDLINE; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry |
| subjects | Aberration Base excision repair Biological Sciences Cisplatin CpG Islands - genetics Damage Deoxyribonucleic acid DNA DNA damage DNA Damage - genetics DNA methylation DNA Methylation - genetics DNA Mismatch Repair - genetics DNA repair DNA Repair - genetics Epithelial cells Epithelial Cells - metabolism Epithelial Cells - virology Epstein-Barr virus Epstein-Barr Virus Infections - genetics Epstein-Barr Virus Infections - pathology Epstein-Barr Virus Infections - virology Gene Expression Regulation - genetics Herpesvirus 4, Human - genetics Herpesvirus 4, Human - pathogenicity Histone Code - genetics Histones Histones - genetics Homologous recombination Homologous Recombination - genetics Homology Humans Mismatch repair MLH1 protein MutL Protein Homolog 1 - genetics Nasopharynx - growth & development Nasopharynx - pathology Nasopharynx - virology PNAS Plus Promoter Regions, Genetic Regulatory mechanisms (biology) Repair Switches Transcription activation Tumorigenesis Viruses |
| title | EBV infection is associated with histone bivalent switch modifications in squamous epithelial cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-06T04%3A20%3A40IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-jstor_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=EBV%20infection%20is%20associated%20with%20histone%20bivalent%20switch%20modifications%20in%20squamous%20epithelial%20cells&rft.jtitle=Proceedings%20of%20the%20National%20Academy%20of%20Sciences%20-%20PNAS&rft.au=Leong,%20Merrin%20Man%20Long&rft.date=2019-07-09&rft.volume=116&rft.issue=28&rft.spage=14144&rft.epage=14153&rft.pages=14144-14153&rft.issn=0027-8424&rft.eissn=1091-6490&rft_id=info:doi/10.1073/pnas.1821752116&rft_dat=%3Cjstor_pubme%3E26760998%3C/jstor_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2268682382&rft_id=info:pmid/31235597&rft_jstor_id=26760998&rfr_iscdi=true |