ARF stimulates XPC to trigger nucleotide excision repair by regulating the repressor complex of E2F4
The tumour suppressor ARF (alternative reading frame), which is mutated or silenced in various tumours, has a crucial role in tumour surveillance to suppress unwarranted cell growth and proliferation. ARF has also been linked to the DNA‐damage‐induced response of p53 because of its ability to inhibi...
Gespeichert in:
| Veröffentlicht in: | EMBO reports 2009-09, Vol.10 (9), p.1036-1042 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1042 |
|---|---|
| container_issue | 9 |
| container_start_page | 1036 |
| container_title | EMBO reports |
| container_volume | 10 |
| creator | Dominguez‐Brauer, Carmen Chen, Yi‐Ju Brauer, Patrick M Pimkina, Julia Raychaudhuri, Pradip |
| description | The tumour suppressor ARF (alternative reading frame), which is mutated or silenced in various tumours, has a crucial role in tumour surveillance to suppress unwarranted cell growth and proliferation. ARF has also been linked to the DNA‐damage‐induced response of p53 because of its ability to inhibit murine double minute 2 (MDM2). Here, however, we provide genetic evidence for a role of ARF in nucleotide excision repair (NER) that is independent of p53. Cells lacking ARF are deficient in NER. Expression of ARF restores the repair activity, which coincides with increased expression of the damaged‐DNA recognition protein xeroderma pigmentosum, complementation group C (XPC). We provide evidence that, by disrupting the interaction between E2F transcription factor 4 (E2F4) and DRTF polypeptide 1 (DP1), ARF reduces the interaction of the E2F4–p130 repressor complex with the promoter of XPC to ensure high‐level expression of XPC. Together, our results point to an important ‘care‐taker’‐type tumour‐suppression function for ARF in NER through the increased expression of XPC. |
| doi_str_mv | 10.1038/embor.2009.139 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2750060</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67619944</sourcerecordid><originalsourceid>FETCH-LOGICAL-c6389-b3a5a59daa9f52e707e279ed28bc3ff846f49b6b1ada36a7e0690c5518348d3e3</originalsourceid><addsrcrecordid>eNqFks9v0zAUxyMEYmNw5YgsDruls2M7ji9IW9UOxPihAmpvlpO8ZB5JXOwE2v8eZ6k2QEI72db7fL9-fl9H0UuCZwTT7Aza3LpZgrGcESofRceEpTKmRGSPD_skIZuj6Jn3NxhjLkX2NDoiMmWMY3wcleerJfK9aYdG9-DR5vMc9Rb1ztQ1ONQNRQO2NyUg2BXGG9shB1ttHMr3YVePMtPVqL-GseDAe-tQYdttAztkK7RIlux59KTSjYcXh_Uk-rZcfJ2_ja8-Xb6bn1_FRUozGedUc81lqbWseAICC0iEhDLJ8oJWVcbSisk8zYkuNU21AJxKXHBOMsqykgI9id5Mvtshb6EsoOudbtTWmVa7vbLaqL8rnblWtf2pEhGGkeJgcHowcPbHAL5XrfEFNI3uwA5epSIlUjL2IJhgyai8dXz9D3hjB9eFKQQmo5xySQM0m6DCWe8dVHctE6zGmNVtzGqMWYWYg-DVnw-9xw-5BkBMwC_TwP4BO7X4cLEaD5P12aT0QdSFP3Df8H-biSeF8T3s7u7S7nuYFxVcrT9eqi_r1QVZb96rjP4GPjbVbA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>208353593</pqid></control><display><type>article</type><title>ARF stimulates XPC to trigger nucleotide excision repair by regulating the repressor complex of E2F4</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Wiley Online Library Free Content</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Dominguez‐Brauer, Carmen ; Chen, Yi‐Ju ; Brauer, Patrick M ; Pimkina, Julia ; Raychaudhuri, Pradip</creator><creatorcontrib>Dominguez‐Brauer, Carmen ; Chen, Yi‐Ju ; Brauer, Patrick M ; Pimkina, Julia ; Raychaudhuri, Pradip</creatorcontrib><description>The tumour suppressor ARF (alternative reading frame), which is mutated or silenced in various tumours, has a crucial role in tumour surveillance to suppress unwarranted cell growth and proliferation. ARF has also been linked to the DNA‐damage‐induced response of p53 because of its ability to inhibit murine double minute 2 (MDM2). Here, however, we provide genetic evidence for a role of ARF in nucleotide excision repair (NER) that is independent of p53. Cells lacking ARF are deficient in NER. Expression of ARF restores the repair activity, which coincides with increased expression of the damaged‐DNA recognition protein xeroderma pigmentosum, complementation group C (XPC). We provide evidence that, by disrupting the interaction between E2F transcription factor 4 (E2F4) and DRTF polypeptide 1 (DP1), ARF reduces the interaction of the E2F4–p130 repressor complex with the promoter of XPC to ensure high‐level expression of XPC. Together, our results point to an important ‘care‐taker’‐type tumour‐suppression function for ARF in NER through the increased expression of XPC.</description><identifier>ISSN: 1469-221X</identifier><identifier>EISSN: 1469-3178</identifier><identifier>DOI: 10.1038/embor.2009.139</identifier><identifier>PMID: 19644500</identifier><identifier>CODEN: ERMEAX</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Animals ; ARF ; Base Sequence ; Cell growth ; Cell Line ; Cyclin-Dependent Kinase Inhibitor p16 - deficiency ; Cyclin-Dependent Kinase Inhibitor p16 - genetics ; Cyclin-Dependent Kinase Inhibitor p16 - metabolism ; Deoxyribonucleic acid ; DNA ; DNA - metabolism ; DNA damage ; DNA Repair ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; E2F4 ; E2F4 Transcription Factor - metabolism ; EMBO13 ; Gene expression ; Gene Expression Regulation ; Mice ; Mice, Knockout ; NER ; p130 ; Protein Binding ; Proteins ; Proto-Oncogene Proteins c-mdm2 - deficiency ; Proto-Oncogene Proteins c-mdm2 - metabolism ; Pyrimidine Dimers - metabolism ; Scientific Report ; Tumor Suppressor Protein p53 - deficiency ; Tumor Suppressor Protein p53 - metabolism ; Tumors ; XPC</subject><ispartof>EMBO reports, 2009-09, Vol.10 (9), p.1036-1042</ispartof><rights>European Molecular Biology Organization 2009</rights><rights>Copyright © 2009 European Molecular Biology Organization</rights><rights>Copyright Nature Publishing Group Sep 2009</rights><rights>Copyright © 2009, European Molecular Biology Organization 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6389-b3a5a59daa9f52e707e279ed28bc3ff846f49b6b1ada36a7e0690c5518348d3e3</citedby><cites>FETCH-LOGICAL-c6389-b3a5a59daa9f52e707e279ed28bc3ff846f49b6b1ada36a7e0690c5518348d3e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2750060/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2750060/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27903,27904,45553,45554,46387,46811,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19644500$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dominguez‐Brauer, Carmen</creatorcontrib><creatorcontrib>Chen, Yi‐Ju</creatorcontrib><creatorcontrib>Brauer, Patrick M</creatorcontrib><creatorcontrib>Pimkina, Julia</creatorcontrib><creatorcontrib>Raychaudhuri, Pradip</creatorcontrib><title>ARF stimulates XPC to trigger nucleotide excision repair by regulating the repressor complex of E2F4</title><title>EMBO reports</title><addtitle>EMBO Rep</addtitle><addtitle>EMBO Rep</addtitle><description>The tumour suppressor ARF (alternative reading frame), which is mutated or silenced in various tumours, has a crucial role in tumour surveillance to suppress unwarranted cell growth and proliferation. ARF has also been linked to the DNA‐damage‐induced response of p53 because of its ability to inhibit murine double minute 2 (MDM2). Here, however, we provide genetic evidence for a role of ARF in nucleotide excision repair (NER) that is independent of p53. Cells lacking ARF are deficient in NER. Expression of ARF restores the repair activity, which coincides with increased expression of the damaged‐DNA recognition protein xeroderma pigmentosum, complementation group C (XPC). We provide evidence that, by disrupting the interaction between E2F transcription factor 4 (E2F4) and DRTF polypeptide 1 (DP1), ARF reduces the interaction of the E2F4–p130 repressor complex with the promoter of XPC to ensure high‐level expression of XPC. Together, our results point to an important ‘care‐taker’‐type tumour‐suppression function for ARF in NER through the increased expression of XPC.</description><subject>Animals</subject><subject>ARF</subject><subject>Base Sequence</subject><subject>Cell growth</subject><subject>Cell Line</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - deficiency</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - genetics</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - metabolism</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA - metabolism</subject><subject>DNA damage</subject><subject>DNA Repair</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>E2F4</subject><subject>E2F4 Transcription Factor - metabolism</subject><subject>EMBO13</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>NER</subject><subject>p130</subject><subject>Protein Binding</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-mdm2 - deficiency</subject><subject>Proto-Oncogene Proteins c-mdm2 - metabolism</subject><subject>Pyrimidine Dimers - metabolism</subject><subject>Scientific Report</subject><subject>Tumor Suppressor Protein p53 - deficiency</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Tumors</subject><subject>XPC</subject><issn>1469-221X</issn><issn>1469-3178</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFks9v0zAUxyMEYmNw5YgsDruls2M7ji9IW9UOxPihAmpvlpO8ZB5JXOwE2v8eZ6k2QEI72db7fL9-fl9H0UuCZwTT7Aza3LpZgrGcESofRceEpTKmRGSPD_skIZuj6Jn3NxhjLkX2NDoiMmWMY3wcleerJfK9aYdG9-DR5vMc9Rb1ztQ1ONQNRQO2NyUg2BXGG9shB1ttHMr3YVePMtPVqL-GseDAe-tQYdttAztkK7RIlux59KTSjYcXh_Uk-rZcfJ2_ja8-Xb6bn1_FRUozGedUc81lqbWseAICC0iEhDLJ8oJWVcbSisk8zYkuNU21AJxKXHBOMsqykgI9id5Mvtshb6EsoOudbtTWmVa7vbLaqL8rnblWtf2pEhGGkeJgcHowcPbHAL5XrfEFNI3uwA5epSIlUjL2IJhgyai8dXz9D3hjB9eFKQQmo5xySQM0m6DCWe8dVHctE6zGmNVtzGqMWYWYg-DVnw-9xw-5BkBMwC_TwP4BO7X4cLEaD5P12aT0QdSFP3Df8H-biSeF8T3s7u7S7nuYFxVcrT9eqi_r1QVZb96rjP4GPjbVbA</recordid><startdate>200909</startdate><enddate>200909</enddate><creator>Dominguez‐Brauer, Carmen</creator><creator>Chen, Yi‐Ju</creator><creator>Brauer, Patrick M</creator><creator>Pimkina, Julia</creator><creator>Raychaudhuri, Pradip</creator><general>John Wiley & Sons, Ltd</general><general>Nature Publishing Group UK</general><general>Blackwell Publishing Ltd</general><general>Nature Publishing Group</general><scope>BSCLL</scope><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>3V.</scope><scope>7QL</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200909</creationdate><title>ARF stimulates XPC to trigger nucleotide excision repair by regulating the repressor complex of E2F4</title><author>Dominguez‐Brauer, Carmen ; Chen, Yi‐Ju ; Brauer, Patrick M ; Pimkina, Julia ; Raychaudhuri, Pradip</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6389-b3a5a59daa9f52e707e279ed28bc3ff846f49b6b1ada36a7e0690c5518348d3e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>ARF</topic><topic>Base Sequence</topic><topic>Cell growth</topic><topic>Cell Line</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - deficiency</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - genetics</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - metabolism</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA - metabolism</topic><topic>DNA damage</topic><topic>DNA Repair</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>E2F4</topic><topic>E2F4 Transcription Factor - metabolism</topic><topic>EMBO13</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>NER</topic><topic>p130</topic><topic>Protein Binding</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-mdm2 - deficiency</topic><topic>Proto-Oncogene Proteins c-mdm2 - metabolism</topic><topic>Pyrimidine Dimers - metabolism</topic><topic>Scientific Report</topic><topic>Tumor Suppressor Protein p53 - deficiency</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Tumors</topic><topic>XPC</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dominguez‐Brauer, Carmen</creatorcontrib><creatorcontrib>Chen, Yi‐Ju</creatorcontrib><creatorcontrib>Brauer, Patrick M</creatorcontrib><creatorcontrib>Pimkina, Julia</creatorcontrib><creatorcontrib>Raychaudhuri, Pradip</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>EMBO reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dominguez‐Brauer, Carmen</au><au>Chen, Yi‐Ju</au><au>Brauer, Patrick M</au><au>Pimkina, Julia</au><au>Raychaudhuri, Pradip</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ARF stimulates XPC to trigger nucleotide excision repair by regulating the repressor complex of E2F4</atitle><jtitle>EMBO reports</jtitle><stitle>EMBO Rep</stitle><addtitle>EMBO Rep</addtitle><date>2009-09</date><risdate>2009</risdate><volume>10</volume><issue>9</issue><spage>1036</spage><epage>1042</epage><pages>1036-1042</pages><issn>1469-221X</issn><eissn>1469-3178</eissn><coden>ERMEAX</coden><abstract>The tumour suppressor ARF (alternative reading frame), which is mutated or silenced in various tumours, has a crucial role in tumour surveillance to suppress unwarranted cell growth and proliferation. ARF has also been linked to the DNA‐damage‐induced response of p53 because of its ability to inhibit murine double minute 2 (MDM2). Here, however, we provide genetic evidence for a role of ARF in nucleotide excision repair (NER) that is independent of p53. Cells lacking ARF are deficient in NER. Expression of ARF restores the repair activity, which coincides with increased expression of the damaged‐DNA recognition protein xeroderma pigmentosum, complementation group C (XPC). We provide evidence that, by disrupting the interaction between E2F transcription factor 4 (E2F4) and DRTF polypeptide 1 (DP1), ARF reduces the interaction of the E2F4–p130 repressor complex with the promoter of XPC to ensure high‐level expression of XPC. Together, our results point to an important ‘care‐taker’‐type tumour‐suppression function for ARF in NER through the increased expression of XPC.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>19644500</pmid><doi>10.1038/embor.2009.139</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1469-221X |
| ispartof | EMBO reports, 2009-09, Vol.10 (9), p.1036-1042 |
| issn | 1469-221X 1469-3178 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2750060 |
| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Wiley Online Library Free Content; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Animals ARF Base Sequence Cell growth Cell Line Cyclin-Dependent Kinase Inhibitor p16 - deficiency Cyclin-Dependent Kinase Inhibitor p16 - genetics Cyclin-Dependent Kinase Inhibitor p16 - metabolism Deoxyribonucleic acid DNA DNA - metabolism DNA damage DNA Repair DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism E2F4 E2F4 Transcription Factor - metabolism EMBO13 Gene expression Gene Expression Regulation Mice Mice, Knockout NER p130 Protein Binding Proteins Proto-Oncogene Proteins c-mdm2 - deficiency Proto-Oncogene Proteins c-mdm2 - metabolism Pyrimidine Dimers - metabolism Scientific Report Tumor Suppressor Protein p53 - deficiency Tumor Suppressor Protein p53 - metabolism Tumors XPC |
| title | ARF stimulates XPC to trigger nucleotide excision repair by regulating the repressor complex of E2F4 |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-26T07%3A53%3A54IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=ARF%20stimulates%20XPC%20to%20trigger%20nucleotide%20excision%20repair%20by%20regulating%20the%20repressor%20complex%20of%20E2F4&rft.jtitle=EMBO%20reports&rft.au=Dominguez%E2%80%90Brauer,%20Carmen&rft.date=2009-09&rft.volume=10&rft.issue=9&rft.spage=1036&rft.epage=1042&rft.pages=1036-1042&rft.issn=1469-221X&rft.eissn=1469-3178&rft.coden=ERMEAX&rft_id=info:doi/10.1038/embor.2009.139&rft_dat=%3Cproquest_pubme%3E67619944%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=208353593&rft_id=info:pmid/19644500&rfr_iscdi=true |