Translesion DNA Synthesis and Carcinogenesis
Tens of thousands of DNA lesions are formed in mammalian cells each day. DNA translesion synthesis is the main mechanism of cell defense against unrepaired DNA lesions. DNA polymerases iota (Pol ι), eta (Pol η), kappa (Pol κ), and zeta (Pol ζ) have active sites that are less stringent toward the DNA...
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Veröffentlicht in: | Biochemistry (Moscow) 2020-04, Vol.85 (4), p.425-435 |
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creator | Shilkin, E. S. Boldinova, E. O. Stolyarenko, A. D. Goncharova, R. I. Chuprov-Netochin, R. N. Khairullin, R. F. Smal, M. P. Makarova, A. V. |
description | Tens of thousands of DNA lesions are formed in mammalian cells each day. DNA translesion synthesis is the main mechanism of cell defense against unrepaired DNA lesions. DNA polymerases iota (Pol ι), eta (Pol η), kappa (Pol κ), and zeta (Pol ζ) have active sites that are less stringent toward the DNA template structure and efficiently incorporate nucleotides opposite DNA lesions. However, these polymerases display low accuracy of DNA synthesis and can introduce mutations in genomic DNA. Impaired functioning of these enzymes can lead to an increased risk of cancer. |
doi_str_mv | 10.1134/S0006297920040033 |
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S. ; Boldinova, E. O. ; Stolyarenko, A. D. ; Goncharova, R. I. ; Chuprov-Netochin, R. N. ; Khairullin, R. F. ; Smal, M. P. ; Makarova, A. V.</creator><creatorcontrib>Shilkin, E. S. ; Boldinova, E. O. ; Stolyarenko, A. D. ; Goncharova, R. I. ; Chuprov-Netochin, R. N. ; Khairullin, R. F. ; Smal, M. P. ; Makarova, A. V.</creatorcontrib><description>Tens of thousands of DNA lesions are formed in mammalian cells each day. DNA translesion synthesis is the main mechanism of cell defense against unrepaired DNA lesions. DNA polymerases iota (Pol ι), eta (Pol η), kappa (Pol κ), and zeta (Pol ζ) have active sites that are less stringent toward the DNA template structure and efficiently incorporate nucleotides opposite DNA lesions. However, these polymerases display low accuracy of DNA synthesis and can introduce mutations in genomic DNA. Impaired functioning of these enzymes can lead to an increased risk of cancer.</description><identifier>ISSN: 0006-2979</identifier><identifier>EISSN: 1608-3040</identifier><identifier>DOI: 10.1134/S0006297920040033</identifier><identifier>PMID: 32569550</identifier><language>eng</language><publisher>Moscow: Pleiades Publishing</publisher><subject>Analysis ; Animals ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Bioorganic Chemistry ; Carcinogenesis ; Carcinogens ; Deoxyribonucleic acid ; DNA ; DNA biosynthesis ; DNA Damage ; DNA Repair ; DNA Replication ; DNA structure ; DNA synthesis ; DNA-directed DNA polymerase ; DNA-Directed DNA Polymerase - metabolism ; Genetic aspects ; Health risks ; Humans ; Lesions ; Life Sciences ; Mammalian cells ; Methods ; Microbiology ; Mutation ; Neoplasms - genetics ; Neoplasms - metabolism ; Neoplasms - pathology ; Nucleotides ; Review</subject><ispartof>Biochemistry (Moscow), 2020-04, Vol.85 (4), p.425-435</ispartof><rights>Pleiades Publishing, Ltd. 2020</rights><rights>COPYRIGHT 2020 Springer</rights><rights>Pleiades Publishing, Ltd. 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c487t-6f093e21598070d2a0fb75e92d54feb41a6501a57074fe9700b0d3e5b849c7b13</citedby><cites>FETCH-LOGICAL-c487t-6f093e21598070d2a0fb75e92d54feb41a6501a57074fe9700b0d3e5b849c7b13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1134/S0006297920040033$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1134/S0006297920040033$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32569550$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shilkin, E. 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S.</au><au>Boldinova, E. O.</au><au>Stolyarenko, A. D.</au><au>Goncharova, R. I.</au><au>Chuprov-Netochin, R. N.</au><au>Khairullin, R. F.</au><au>Smal, M. P.</au><au>Makarova, A. V.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Translesion DNA Synthesis and Carcinogenesis</atitle><jtitle>Biochemistry (Moscow)</jtitle><stitle>Biochemistry Moscow</stitle><addtitle>Biochemistry (Mosc)</addtitle><date>2020-04-01</date><risdate>2020</risdate><volume>85</volume><issue>4</issue><spage>425</spage><epage>435</epage><pages>425-435</pages><issn>0006-2979</issn><eissn>1608-3040</eissn><abstract>Tens of thousands of DNA lesions are formed in mammalian cells each day. DNA translesion synthesis is the main mechanism of cell defense against unrepaired DNA lesions. DNA polymerases iota (Pol ι), eta (Pol η), kappa (Pol κ), and zeta (Pol ζ) have active sites that are less stringent toward the DNA template structure and efficiently incorporate nucleotides opposite DNA lesions. However, these polymerases display low accuracy of DNA synthesis and can introduce mutations in genomic DNA. Impaired functioning of these enzymes can lead to an increased risk of cancer.</abstract><cop>Moscow</cop><pub>Pleiades Publishing</pub><pmid>32569550</pmid><doi>10.1134/S0006297920040033</doi><tpages>11</tpages></addata></record> |
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subjects | Analysis Animals Biochemistry Biomedical and Life Sciences Biomedicine Bioorganic Chemistry Carcinogenesis Carcinogens Deoxyribonucleic acid DNA DNA biosynthesis DNA Damage DNA Repair DNA Replication DNA structure DNA synthesis DNA-directed DNA polymerase DNA-Directed DNA Polymerase - metabolism Genetic aspects Health risks Humans Lesions Life Sciences Mammalian cells Methods Microbiology Mutation Neoplasms - genetics Neoplasms - metabolism Neoplasms - pathology Nucleotides Review |
title | Translesion DNA Synthesis and Carcinogenesis |
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