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dc.contributor.authorNowosielska, Anetta
dc.date2022-08-11T08:09:32.000
dc.date.accessioned2022-08-23T16:34:34Z
dc.date.available2022-08-23T16:34:34Z
dc.date.issued2007-09-26
dc.date.submitted2009-03-16
dc.identifier.citationActa Biochim Pol. 2007;54(3):483-94. Epub 2007 Sep 23.
dc.identifier.issn0001-527X (Print)
dc.identifier.pmid17893749
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38362
dc.description.abstractRecombinational repair is a well conserved DNA repair mechanism present in all living organisms. Repair by homologous recombination is generally accurate as it uses undamaged homologous DNA molecule as a repair template. In Escherichia coli homologous recombination repairs both the double-strand breaks and single-strand gaps in DNA. DNA double-strand breaks (DSB) can be induced upon exposure to exogenous sources such as ionizing radiation or endogenous DNA-damaging agents including reactive oxygen species (ROS) as well as during natural biological processes like conjugation. However, the bulk of double strand breaks are formed during replication fork collapse encountering an unrepaired single strand gap in DNA. Under such circumstances DNA replication on the damaged template can be resumed only if supported by homologous recombination. This functional cooperation of homologous recombination with replication machinery enables successful completion of genome duplication and faithful transmission of genetic material to a daughter cell. In eukaryotes, homologous recombination is also involved in essential biological processes such as preservation of genome integrity, DNA damage checkpoint activation, DNA damage repair, DNA replication, mating type switching, transposition, immune system development and meiosis. When unregulated, recombination can lead to genome instability and carcinogenesis.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=17893749&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://www.actabp.pl/pdf/3_2007/483.pdf
dc.subjectAnimals
dc.subjectBacterial Proteins
dc.subjectDNA Repair
dc.subjectEscherichia coli
dc.subjectGenomic Instability
dc.subjectHumans
dc.subjectModels, Genetic
dc.subjectRecombination, Genetic
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleBacterial DNA repair genes and their eukaryotic homologues: 5. The role of recombination in DNA repair and genome stability
dc.typeJournal Article
dc.source.journaltitleActa biochimica Polonica
dc.source.volume54
dc.source.issue3
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1226
dc.identifier.contextkey782892
html.description.abstract<p>Recombinational repair is a well conserved DNA repair mechanism present in all living organisms. Repair by homologous recombination is generally accurate as it uses undamaged homologous DNA molecule as a repair template. In Escherichia coli homologous recombination repairs both the double-strand breaks and single-strand gaps in DNA. DNA double-strand breaks (DSB) can be induced upon exposure to exogenous sources such as ionizing radiation or endogenous DNA-damaging agents including reactive oxygen species (ROS) as well as during natural biological processes like conjugation. However, the bulk of double strand breaks are formed during replication fork collapse encountering an unrepaired single strand gap in DNA. Under such circumstances DNA replication on the damaged template can be resumed only if supported by homologous recombination. This functional cooperation of homologous recombination with replication machinery enables successful completion of genome duplication and faithful transmission of genetic material to a daughter cell. In eukaryotes, homologous recombination is also involved in essential biological processes such as preservation of genome integrity, DNA damage checkpoint activation, DNA damage repair, DNA replication, mating type switching, transposition, immune system development and meiosis. When unregulated, recombination can lead to genome instability and carcinogenesis.</p>
dc.identifier.submissionpathoapubs/1226
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages483-94


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