Chromosomal protein HMGN1 enhances the rate of DNA repair in chromatin
We report that HMGN1, a nucleosome binding protein that destabilizes the higher‐order chromatin structure, modulates the repair rate of ultraviolet light (UV)‐induced DNA lesions in chromatin. Hmgn1 −/− mouse embryonic fibroblasts (MEFs) are hypersensitive to UV, and the removal rate of photoproduct...
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| Veröffentlicht in: | The EMBO journal 2003-04, Vol.22 (7), p.1665-1675 |
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| creator | Birger, Yehudit West, Katherine L. Postnikov, Yuri V. Lim, Jae-Hwan Furusawa, Takashi Wagner, James P. Laufer, Craig S. Kraemer, Kenneth H. Bustin, Michael |
| description | We report that HMGN1, a nucleosome binding protein that destabilizes the higher‐order chromatin structure, modulates the repair rate of ultraviolet light (UV)‐induced DNA lesions in chromatin.
Hmgn1
−/−
mouse embryonic fibroblasts (MEFs) are hypersensitive to UV, and the removal rate of photoproducts from the chromatin of
Hmgn1
−/−
MEFs is decreased as compared with the chromatin of
Hmgn1
+/+
MEFs; yet, host cell reactivation assays and DNA array analysis indicate that the nucleotide excision repair (NER) pathway in the
Hmgn1
−/−
MEFs remains intact. The UV hypersensitivity of
Hmgn1
−/−
MEFs could be rescued by transfection with plasmids expressing wild‐type HMGN1 protein, but not with plasmids expressing HMGN1 mutants that do not bind to nucleosomes or do not unfold chromatin. Transcriptionally active genes, the main target of the NER pathways in mice, contain HMGN1 protein, and loss of HMGN1 protein reduces the accessibility of transcribed genes to nucleases. By reducing the compaction of the higher‐order chromatin structure, HMGN1 facilitates access to UV‐damaged DNA sites and enhances the rate of DNA repair in chromatin. |
| doi_str_mv | 10.1093/emboj/cdg142 |
| format | Article |
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Hmgn1
−/−
mouse embryonic fibroblasts (MEFs) are hypersensitive to UV, and the removal rate of photoproducts from the chromatin of
Hmgn1
−/−
MEFs is decreased as compared with the chromatin of
Hmgn1
+/+
MEFs; yet, host cell reactivation assays and DNA array analysis indicate that the nucleotide excision repair (NER) pathway in the
Hmgn1
−/−
MEFs remains intact. The UV hypersensitivity of
Hmgn1
−/−
MEFs could be rescued by transfection with plasmids expressing wild‐type HMGN1 protein, but not with plasmids expressing HMGN1 mutants that do not bind to nucleosomes or do not unfold chromatin. Transcriptionally active genes, the main target of the NER pathways in mice, contain HMGN1 protein, and loss of HMGN1 protein reduces the accessibility of transcribed genes to nucleases. By reducing the compaction of the higher‐order chromatin structure, HMGN1 facilitates access to UV‐damaged DNA sites and enhances the rate of DNA repair in chromatin.</description><identifier>ISSN: 0261-4189</identifier><identifier>ISSN: 1460-2075</identifier><identifier>EISSN: 1460-2075</identifier><identifier>DOI: 10.1093/emboj/cdg142</identifier><identifier>PMID: 12660172</identifier><identifier>CODEN: EMJODG</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Animals ; chromatin ; Chromatin - genetics ; chromosomal proteins ; Deoxyribonucleic acid ; DNA ; DNA Repair - physiology ; EMBO09 ; EMBO13 ; Embryo, Mammalian - cytology ; Embryo, Mammalian - metabolism ; Fibroblasts - metabolism ; Gene Expression Profiling ; HMGN ; HMGN1 Protein - physiology ; Hypersensitivity ; knockout mouse ; Mice ; Mice, Mutant Strains ; Precipitin Tests ; Skin - cytology ; Skin - metabolism ; Skin - radiation effects ; Ultraviolet radiation ; UV repair</subject><ispartof>The EMBO journal, 2003-04, Vol.22 (7), p.1665-1675</ispartof><rights>European Molecular Biology Organization 2003</rights><rights>Copyright © 2003 European Molecular Biology Organization</rights><rights>Copyright Oxford University Press(England) Apr 01, 2003</rights><rights>Copyright © 2003 European Molecular Biology Organization 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6473-c77fa818d5a1ac446f7b3a493a24db38200c567dc612aceae4c0e4d7109eb6a83</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC152887/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC152887/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,1417,1433,27924,27925,45574,45575,46409,46833,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12660172$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Birger, Yehudit</creatorcontrib><creatorcontrib>West, Katherine L.</creatorcontrib><creatorcontrib>Postnikov, Yuri V.</creatorcontrib><creatorcontrib>Lim, Jae-Hwan</creatorcontrib><creatorcontrib>Furusawa, Takashi</creatorcontrib><creatorcontrib>Wagner, James P.</creatorcontrib><creatorcontrib>Laufer, Craig S.</creatorcontrib><creatorcontrib>Kraemer, Kenneth H.</creatorcontrib><creatorcontrib>Bustin, Michael</creatorcontrib><title>Chromosomal protein HMGN1 enhances the rate of DNA repair in chromatin</title><title>The EMBO journal</title><addtitle>EMBO J</addtitle><addtitle>EMBO J</addtitle><description>We report that HMGN1, a nucleosome binding protein that destabilizes the higher‐order chromatin structure, modulates the repair rate of ultraviolet light (UV)‐induced DNA lesions in chromatin.
Hmgn1
−/−
mouse embryonic fibroblasts (MEFs) are hypersensitive to UV, and the removal rate of photoproducts from the chromatin of
Hmgn1
−/−
MEFs is decreased as compared with the chromatin of
Hmgn1
+/+
MEFs; yet, host cell reactivation assays and DNA array analysis indicate that the nucleotide excision repair (NER) pathway in the
Hmgn1
−/−
MEFs remains intact. The UV hypersensitivity of
Hmgn1
−/−
MEFs could be rescued by transfection with plasmids expressing wild‐type HMGN1 protein, but not with plasmids expressing HMGN1 mutants that do not bind to nucleosomes or do not unfold chromatin. Transcriptionally active genes, the main target of the NER pathways in mice, contain HMGN1 protein, and loss of HMGN1 protein reduces the accessibility of transcribed genes to nucleases. By reducing the compaction of the higher‐order chromatin structure, HMGN1 facilitates access to UV‐damaged DNA sites and enhances the rate of DNA repair in chromatin.</description><subject>Animals</subject><subject>chromatin</subject><subject>Chromatin - genetics</subject><subject>chromosomal proteins</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Repair - physiology</subject><subject>EMBO09</subject><subject>EMBO13</subject><subject>Embryo, Mammalian - cytology</subject><subject>Embryo, Mammalian - metabolism</subject><subject>Fibroblasts - metabolism</subject><subject>Gene Expression Profiling</subject><subject>HMGN</subject><subject>HMGN1 Protein - physiology</subject><subject>Hypersensitivity</subject><subject>knockout mouse</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Precipitin Tests</subject><subject>Skin - cytology</subject><subject>Skin - metabolism</subject><subject>Skin - radiation effects</subject><subject>Ultraviolet radiation</subject><subject>UV repair</subject><issn>0261-4189</issn><issn>1460-2075</issn><issn>1460-2075</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</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>eNqFkUtv1DAUhSMEotPCji0oYtEVoX47WbAo084U1A6qBHRpOc7NTIbEHuwE6L_HQ0ZDeQhWXtzvHJ97T5I8weglRgU9ga506xNTLTEj95IJZgJlBEl-P5kgInDGcF4cJIchrBFCPJf4YXKAiRAISzJJZtOVd50LrtNtuvGuh8amF1fzBU7BrrQ1ENJ-BanXPaSuTs8Wp6mHjW58GkGzFeu-sY-SB7VuAzzevUfJh9n5--lFdvlu_mZ6epkZwSTNjJS1znFecY21YUzUsqSaFVQTVpU0JwgZLmRlBCbagAZmELBKxkWhFDqnR8mr0XczlB1UBmzvdas2vum0v1VON-rXiW1Waum-KMxJnsuoP97pvfs8QOhV1wQDbastuCEoSTEuCl78F8TRTBK6dXz-G7h2g7fxCAoXnPCCERqhFyNkvAvBQ71PjJHatqh-tKjGFiP-7O6WP-FdbRHgI_C1aeH2n2bq_Or1W8kLjvg2RzbqQpTYJfg7Yf8e5OnIW90PHvYf_eHXhB6-7cfaf1Ii3oerm8Vcza5nN9dnH6ki9DvKtNMH</recordid><startdate>20030401</startdate><enddate>20030401</enddate><creator>Birger, Yehudit</creator><creator>West, Katherine L.</creator><creator>Postnikov, Yuri V.</creator><creator>Lim, Jae-Hwan</creator><creator>Furusawa, Takashi</creator><creator>Wagner, James P.</creator><creator>Laufer, Craig S.</creator><creator>Kraemer, Kenneth H.</creator><creator>Bustin, Michael</creator><general>John Wiley & Sons, Ltd</general><general>Nature Publishing Group UK</general><general>Blackwell Publishing Ltd</general><general>Oxford University Press</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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</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>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BKSAR</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>PCBAR</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>20030401</creationdate><title>Chromosomal protein HMGN1 enhances the rate of DNA repair in chromatin</title><author>Birger, Yehudit ; West, Katherine L. ; Postnikov, Yuri V. ; Lim, Jae-Hwan ; Furusawa, Takashi ; Wagner, James P. ; Laufer, Craig S. ; Kraemer, Kenneth H. ; Bustin, Michael</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6473-c77fa818d5a1ac446f7b3a493a24db38200c567dc612aceae4c0e4d7109eb6a83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>chromatin</topic><topic>Chromatin - genetics</topic><topic>chromosomal proteins</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA Repair - physiology</topic><topic>EMBO09</topic><topic>EMBO13</topic><topic>Embryo, Mammalian - cytology</topic><topic>Embryo, Mammalian - metabolism</topic><topic>Fibroblasts - metabolism</topic><topic>Gene Expression Profiling</topic><topic>HMGN</topic><topic>HMGN1 Protein - physiology</topic><topic>Hypersensitivity</topic><topic>knockout mouse</topic><topic>Mice</topic><topic>Mice, Mutant Strains</topic><topic>Precipitin Tests</topic><topic>Skin - cytology</topic><topic>Skin - metabolism</topic><topic>Skin - radiation effects</topic><topic>Ultraviolet radiation</topic><topic>UV repair</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Birger, Yehudit</creatorcontrib><creatorcontrib>West, Katherine L.</creatorcontrib><creatorcontrib>Postnikov, Yuri V.</creatorcontrib><creatorcontrib>Lim, Jae-Hwan</creatorcontrib><creatorcontrib>Furusawa, Takashi</creatorcontrib><creatorcontrib>Wagner, James P.</creatorcontrib><creatorcontrib>Laufer, Craig S.</creatorcontrib><creatorcontrib>Kraemer, Kenneth H.</creatorcontrib><creatorcontrib>Bustin, Michael</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>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</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>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 Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Earth, Atmospheric & Aquatic 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>Earth, Atmospheric & Aquatic Science Database</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>The EMBO journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Birger, Yehudit</au><au>West, Katherine L.</au><au>Postnikov, Yuri V.</au><au>Lim, Jae-Hwan</au><au>Furusawa, Takashi</au><au>Wagner, James P.</au><au>Laufer, Craig S.</au><au>Kraemer, Kenneth H.</au><au>Bustin, Michael</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chromosomal protein HMGN1 enhances the rate of DNA repair in chromatin</atitle><jtitle>The EMBO journal</jtitle><stitle>EMBO J</stitle><addtitle>EMBO J</addtitle><date>2003-04-01</date><risdate>2003</risdate><volume>22</volume><issue>7</issue><spage>1665</spage><epage>1675</epage><pages>1665-1675</pages><issn>0261-4189</issn><issn>1460-2075</issn><eissn>1460-2075</eissn><coden>EMJODG</coden><abstract>We report that HMGN1, a nucleosome binding protein that destabilizes the higher‐order chromatin structure, modulates the repair rate of ultraviolet light (UV)‐induced DNA lesions in chromatin.
Hmgn1
−/−
mouse embryonic fibroblasts (MEFs) are hypersensitive to UV, and the removal rate of photoproducts from the chromatin of
Hmgn1
−/−
MEFs is decreased as compared with the chromatin of
Hmgn1
+/+
MEFs; yet, host cell reactivation assays and DNA array analysis indicate that the nucleotide excision repair (NER) pathway in the
Hmgn1
−/−
MEFs remains intact. The UV hypersensitivity of
Hmgn1
−/−
MEFs could be rescued by transfection with plasmids expressing wild‐type HMGN1 protein, but not with plasmids expressing HMGN1 mutants that do not bind to nucleosomes or do not unfold chromatin. Transcriptionally active genes, the main target of the NER pathways in mice, contain HMGN1 protein, and loss of HMGN1 protein reduces the accessibility of transcribed genes to nucleases. By reducing the compaction of the higher‐order chromatin structure, HMGN1 facilitates access to UV‐damaged DNA sites and enhances the rate of DNA repair in chromatin.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>12660172</pmid><doi>10.1093/emboj/cdg142</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 0261-4189 1460-2075 1460-2075 |
| language | eng |
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| source | Wiley Online Library - AutoHoldings Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Animals chromatin Chromatin - genetics chromosomal proteins Deoxyribonucleic acid DNA DNA Repair - physiology EMBO09 EMBO13 Embryo, Mammalian - cytology Embryo, Mammalian - metabolism Fibroblasts - metabolism Gene Expression Profiling HMGN HMGN1 Protein - physiology Hypersensitivity knockout mouse Mice Mice, Mutant Strains Precipitin Tests Skin - cytology Skin - metabolism Skin - radiation effects Ultraviolet radiation UV repair |
| title | Chromosomal protein HMGN1 enhances the rate of DNA repair in chromatin |
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