Potential roles for p53 in nucleotide excision repair
Ultraviolet (UV) light-induced DNA damage is repaired by the nucleotide excision repair pathway, which can be subdivided into transcription-coupled repair (TCR) and global genome repair (GGR). Treatment of cells with a priming dose of UV light appears to stimulate both GGR and TCR, suggesting that t...
Gespeichert in:
| Veröffentlicht in: | Carcinogenesis (New York) 1999-08, Vol.20 (8), p.1389-1396 |
|---|---|
| Hauptverfasser: | , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1396 |
|---|---|
| container_issue | 8 |
| container_start_page | 1389 |
| container_title | Carcinogenesis (New York) |
| container_volume | 20 |
| creator | McKay, Bruce C. Ljungman, Mats Rainbow, Andrew J. |
| description | Ultraviolet (UV) light-induced DNA damage is repaired by the nucleotide excision repair pathway, which can be subdivided into transcription-coupled repair (TCR) and global genome repair (GGR). Treatment of cells with a priming dose of UV light appears to stimulate both GGR and TCR, suggesting that these processes are inducible. GGR appears to be disrupted in p53-deficient fibroblasts, whereas the effect of p53 disruption on TCR remains somewhat controversial. Normal recovery of mRNA synthesis following UV irradiation is thought to depend on TCR. We have found that the recovery of mRNA synthesis following exposure to UV light is severely attenuated in p53-deficient human fibroblasts. Therefore, p53 disruption may lead to a defect in TCR or a post-repair process required for the recovery of mRNA synthesis. Several different functions of p53 have been proposed which could contribute to these cellular processes. We suggest that p53 could participate in GGR and the recovery of mRNA synthesis following UV exposure through the regulation of steady-state levels of one or more p53-regulated gene products important for these processes. Furthermore, we suggest that the role of p53 in the recovery of mRNA synthesis is important for resistance to UV-induced apoptosis. |
| doi_str_mv | 10.1093/carcin/20.8.1389 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_17911621</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>17500691</sourcerecordid><originalsourceid>FETCH-LOGICAL-c455t-d364215aee17322a20f47fe0ad3225c2ff1a5a5e980f792319f92c75668809a13</originalsourceid><addsrcrecordid>eNqN0M9LHDEUwPFQWupqe-9J5lC8zfpefudYpFVRqgeF4iWk2RdInZ3ZJrOg_70js6hHT-GRz3uHL2PfEJYIThzHUGLujzks7RKFdR_YAqWGlqOFj2wBKEUrhJB7bL_WfwCohXKf2R6C5NpYvmDqehipH3PomjJ0VJs0lGajRJP7pt_GjoYxr6ihh5hrHvqm0Cbk8oV9SqGr9HX3HrDbXz9vTs7ay6vT85Mfl22USo3tSmjJUQUiNILzwCFJkwjCappU5ClhUEGRs5CM4wJdcjwapbW14AKKA3Y0392U4f-W6ujXuUbqutDTsK0ejUPU_D1QAWj3HsitdE5PEGYYy1BroeQ3Ja9DefQI_jm-n-N7Dt765_jTyuHu9vbvmlZvFubaE_i-A6HG0KUS-inrq3NoUNqJtTPLdaSHl-9Q7r02wih_9ufOu9-n1_ZOK38hngAiVpqE</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>17284996</pqid></control><display><type>article</type><title>Potential roles for p53 in nucleotide excision repair</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Oxford University Press Journals All Titles (1996-Current)</source><source>Alma/SFX Local Collection</source><creator>McKay, Bruce C. ; Ljungman, Mats ; Rainbow, Andrew J.</creator><creatorcontrib>McKay, Bruce C. ; Ljungman, Mats ; Rainbow, Andrew J.</creatorcontrib><description>Ultraviolet (UV) light-induced DNA damage is repaired by the nucleotide excision repair pathway, which can be subdivided into transcription-coupled repair (TCR) and global genome repair (GGR). Treatment of cells with a priming dose of UV light appears to stimulate both GGR and TCR, suggesting that these processes are inducible. GGR appears to be disrupted in p53-deficient fibroblasts, whereas the effect of p53 disruption on TCR remains somewhat controversial. Normal recovery of mRNA synthesis following UV irradiation is thought to depend on TCR. We have found that the recovery of mRNA synthesis following exposure to UV light is severely attenuated in p53-deficient human fibroblasts. Therefore, p53 disruption may lead to a defect in TCR or a post-repair process required for the recovery of mRNA synthesis. Several different functions of p53 have been proposed which could contribute to these cellular processes. We suggest that p53 could participate in GGR and the recovery of mRNA synthesis following UV exposure through the regulation of steady-state levels of one or more p53-regulated gene products important for these processes. Furthermore, we suggest that the role of p53 in the recovery of mRNA synthesis is important for resistance to UV-induced apoptosis.</description><identifier>ISSN: 0143-3334</identifier><identifier>ISSN: 1460-2180</identifier><identifier>EISSN: 1460-2180</identifier><identifier>DOI: 10.1093/carcin/20.8.1389</identifier><identifier>PMID: 10426782</identifier><identifier>CODEN: CRNGDP</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Biological and medical sciences ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Cockayne syndrome ; Cockayne Syndrome - genetics ; CPD ; cyclobutane pyrimidine dimers ; DNA - radiation effects ; DNA Repair - genetics ; DNA Repair - radiation effects ; Fibroblasts - radiation effects ; Fundamental and applied biological sciences. Psychology ; Genes, p53 - genetics ; Genes, Reporter - genetics ; Genetic Vectors - administration & dosage ; GGR ; global genome repair ; HCR ; host cell reactivation ; Hot Temperature ; HPV-E6 ; human papilloma virus 16 E6 ; Humans ; LFS ; Li–Fraumeni syndrome ; Molecular and cellular biology ; mRNA biosynthesis ; NER ; nucleotide excision repair ; recovery of mRNA synthesis ; RNA, Messenger - biosynthesis ; RRS ; TCR ; Transcription, Genetic - genetics ; Transcription, Genetic - radiation effects ; transcription-coupled repair ; Transfection ; Tumor Suppressor Protein p53 - physiology ; ultraviolet ; Ultraviolet Rays ; xeroderma pigmentosum ; Xeroderma Pigmentosum - genetics</subject><ispartof>Carcinogenesis (New York), 1999-08, Vol.20 (8), p.1389-1396</ispartof><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-d364215aee17322a20f47fe0ad3225c2ff1a5a5e980f792319f92c75668809a13</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1917148$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10426782$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>McKay, Bruce C.</creatorcontrib><creatorcontrib>Ljungman, Mats</creatorcontrib><creatorcontrib>Rainbow, Andrew J.</creatorcontrib><title>Potential roles for p53 in nucleotide excision repair</title><title>Carcinogenesis (New York)</title><addtitle>Carcinogenesis</addtitle><description>Ultraviolet (UV) light-induced DNA damage is repaired by the nucleotide excision repair pathway, which can be subdivided into transcription-coupled repair (TCR) and global genome repair (GGR). Treatment of cells with a priming dose of UV light appears to stimulate both GGR and TCR, suggesting that these processes are inducible. GGR appears to be disrupted in p53-deficient fibroblasts, whereas the effect of p53 disruption on TCR remains somewhat controversial. Normal recovery of mRNA synthesis following UV irradiation is thought to depend on TCR. We have found that the recovery of mRNA synthesis following exposure to UV light is severely attenuated in p53-deficient human fibroblasts. Therefore, p53 disruption may lead to a defect in TCR or a post-repair process required for the recovery of mRNA synthesis. Several different functions of p53 have been proposed which could contribute to these cellular processes. We suggest that p53 could participate in GGR and the recovery of mRNA synthesis following UV exposure through the regulation of steady-state levels of one or more p53-regulated gene products important for these processes. Furthermore, we suggest that the role of p53 in the recovery of mRNA synthesis is important for resistance to UV-induced apoptosis.</description><subject>Biological and medical sciences</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Cockayne syndrome</subject><subject>Cockayne Syndrome - genetics</subject><subject>CPD</subject><subject>cyclobutane pyrimidine dimers</subject><subject>DNA - radiation effects</subject><subject>DNA Repair - genetics</subject><subject>DNA Repair - radiation effects</subject><subject>Fibroblasts - radiation effects</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genes, p53 - genetics</subject><subject>Genes, Reporter - genetics</subject><subject>Genetic Vectors - administration & dosage</subject><subject>GGR</subject><subject>global genome repair</subject><subject>HCR</subject><subject>host cell reactivation</subject><subject>Hot Temperature</subject><subject>HPV-E6</subject><subject>human papilloma virus 16 E6</subject><subject>Humans</subject><subject>LFS</subject><subject>Li–Fraumeni syndrome</subject><subject>Molecular and cellular biology</subject><subject>mRNA biosynthesis</subject><subject>NER</subject><subject>nucleotide excision repair</subject><subject>recovery of mRNA synthesis</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RRS</subject><subject>TCR</subject><subject>Transcription, Genetic - genetics</subject><subject>Transcription, Genetic - radiation effects</subject><subject>transcription-coupled repair</subject><subject>Transfection</subject><subject>Tumor Suppressor Protein p53 - physiology</subject><subject>ultraviolet</subject><subject>Ultraviolet Rays</subject><subject>xeroderma pigmentosum</subject><subject>Xeroderma Pigmentosum - genetics</subject><issn>0143-3334</issn><issn>1460-2180</issn><issn>1460-2180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqN0M9LHDEUwPFQWupqe-9J5lC8zfpefudYpFVRqgeF4iWk2RdInZ3ZJrOg_70js6hHT-GRz3uHL2PfEJYIThzHUGLujzks7RKFdR_YAqWGlqOFj2wBKEUrhJB7bL_WfwCohXKf2R6C5NpYvmDqehipH3PomjJ0VJs0lGajRJP7pt_GjoYxr6ihh5hrHvqm0Cbk8oV9SqGr9HX3HrDbXz9vTs7ay6vT85Mfl22USo3tSmjJUQUiNILzwCFJkwjCappU5ClhUEGRs5CM4wJdcjwapbW14AKKA3Y0392U4f-W6ujXuUbqutDTsK0ejUPU_D1QAWj3HsitdE5PEGYYy1BroeQ3Ja9DefQI_jm-n-N7Dt765_jTyuHu9vbvmlZvFubaE_i-A6HG0KUS-inrq3NoUNqJtTPLdaSHl-9Q7r02wih_9ufOu9-n1_ZOK38hngAiVpqE</recordid><startdate>19990801</startdate><enddate>19990801</enddate><creator>McKay, Bruce C.</creator><creator>Ljungman, Mats</creator><creator>Rainbow, Andrew J.</creator><general>Oxford University Press</general><scope>BSCLL</scope><scope>IQODW</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>7TO</scope><scope>H94</scope><scope>7TM</scope></search><sort><creationdate>19990801</creationdate><title>Potential roles for p53 in nucleotide excision repair</title><author>McKay, Bruce C. ; Ljungman, Mats ; Rainbow, Andrew J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-d364215aee17322a20f47fe0ad3225c2ff1a5a5e980f792319f92c75668809a13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Biological and medical sciences</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Cockayne syndrome</topic><topic>Cockayne Syndrome - genetics</topic><topic>CPD</topic><topic>cyclobutane pyrimidine dimers</topic><topic>DNA - radiation effects</topic><topic>DNA Repair - genetics</topic><topic>DNA Repair - radiation effects</topic><topic>Fibroblasts - radiation effects</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genes, p53 - genetics</topic><topic>Genes, Reporter - genetics</topic><topic>Genetic Vectors - administration & dosage</topic><topic>GGR</topic><topic>global genome repair</topic><topic>HCR</topic><topic>host cell reactivation</topic><topic>Hot Temperature</topic><topic>HPV-E6</topic><topic>human papilloma virus 16 E6</topic><topic>Humans</topic><topic>LFS</topic><topic>Li–Fraumeni syndrome</topic><topic>Molecular and cellular biology</topic><topic>mRNA biosynthesis</topic><topic>NER</topic><topic>nucleotide excision repair</topic><topic>recovery of mRNA synthesis</topic><topic>RNA, Messenger - biosynthesis</topic><topic>RRS</topic><topic>TCR</topic><topic>Transcription, Genetic - genetics</topic><topic>Transcription, Genetic - radiation effects</topic><topic>transcription-coupled repair</topic><topic>Transfection</topic><topic>Tumor Suppressor Protein p53 - physiology</topic><topic>ultraviolet</topic><topic>Ultraviolet Rays</topic><topic>xeroderma pigmentosum</topic><topic>Xeroderma Pigmentosum - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McKay, Bruce C.</creatorcontrib><creatorcontrib>Ljungman, Mats</creatorcontrib><creatorcontrib>Rainbow, Andrew J.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Nucleic Acids Abstracts</collection><jtitle>Carcinogenesis (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>McKay, Bruce C.</au><au>Ljungman, Mats</au><au>Rainbow, Andrew J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Potential roles for p53 in nucleotide excision repair</atitle><jtitle>Carcinogenesis (New York)</jtitle><addtitle>Carcinogenesis</addtitle><date>1999-08-01</date><risdate>1999</risdate><volume>20</volume><issue>8</issue><spage>1389</spage><epage>1396</epage><pages>1389-1396</pages><issn>0143-3334</issn><issn>1460-2180</issn><eissn>1460-2180</eissn><coden>CRNGDP</coden><abstract>Ultraviolet (UV) light-induced DNA damage is repaired by the nucleotide excision repair pathway, which can be subdivided into transcription-coupled repair (TCR) and global genome repair (GGR). Treatment of cells with a priming dose of UV light appears to stimulate both GGR and TCR, suggesting that these processes are inducible. GGR appears to be disrupted in p53-deficient fibroblasts, whereas the effect of p53 disruption on TCR remains somewhat controversial. Normal recovery of mRNA synthesis following UV irradiation is thought to depend on TCR. We have found that the recovery of mRNA synthesis following exposure to UV light is severely attenuated in p53-deficient human fibroblasts. Therefore, p53 disruption may lead to a defect in TCR or a post-repair process required for the recovery of mRNA synthesis. Several different functions of p53 have been proposed which could contribute to these cellular processes. We suggest that p53 could participate in GGR and the recovery of mRNA synthesis following UV exposure through the regulation of steady-state levels of one or more p53-regulated gene products important for these processes. Furthermore, we suggest that the role of p53 in the recovery of mRNA synthesis is important for resistance to UV-induced apoptosis.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>10426782</pmid><doi>10.1093/carcin/20.8.1389</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0143-3334 |
| ispartof | Carcinogenesis (New York), 1999-08, Vol.20 (8), p.1389-1396 |
| issn | 0143-3334 1460-2180 1460-2180 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_17911621 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Oxford University Press Journals All Titles (1996-Current); Alma/SFX Local Collection |
| subjects | Biological and medical sciences Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Cockayne syndrome Cockayne Syndrome - genetics CPD cyclobutane pyrimidine dimers DNA - radiation effects DNA Repair - genetics DNA Repair - radiation effects Fibroblasts - radiation effects Fundamental and applied biological sciences. Psychology Genes, p53 - genetics Genes, Reporter - genetics Genetic Vectors - administration & dosage GGR global genome repair HCR host cell reactivation Hot Temperature HPV-E6 human papilloma virus 16 E6 Humans LFS Li–Fraumeni syndrome Molecular and cellular biology mRNA biosynthesis NER nucleotide excision repair recovery of mRNA synthesis RNA, Messenger - biosynthesis RRS TCR Transcription, Genetic - genetics Transcription, Genetic - radiation effects transcription-coupled repair Transfection Tumor Suppressor Protein p53 - physiology ultraviolet Ultraviolet Rays xeroderma pigmentosum Xeroderma Pigmentosum - genetics |
| title | Potential roles for p53 in nucleotide excision repair |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-18T04%3A32%3A16IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Potential%20roles%20for%20p53%20in%20nucleotide%20excision%20repair&rft.jtitle=Carcinogenesis%20(New%20York)&rft.au=McKay,%20Bruce%20C.&rft.date=1999-08-01&rft.volume=20&rft.issue=8&rft.spage=1389&rft.epage=1396&rft.pages=1389-1396&rft.issn=0143-3334&rft.eissn=1460-2180&rft.coden=CRNGDP&rft_id=info:doi/10.1093/carcin/20.8.1389&rft_dat=%3Cproquest_cross%3E17500691%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=17284996&rft_id=info:pmid/10426782&rfr_iscdi=true |