untitled
<OAI-PMH schemaLocation=http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd>
<responseDate>2018-01-17T12:16:51Z</responseDate>
<request identifier=oai:HAL:hal-01680533v1 verb=GetRecord metadataPrefix=oai_dc>http://api.archives-ouvertes.fr/oai/hal/</request>
<GetRecord>
<record>
<header>
<identifier>oai:HAL:hal-01680533v1</identifier>
<datestamp>2018-01-11</datestamp>
<setSpec>type:ART</setSpec>
<setSpec>subject:sde</setSpec>
<setSpec>subject:sdv</setSpec>
<setSpec>collection:UNIV-AG</setSpec>
<setSpec>collection:SDE</setSpec>
<setSpec>collection:GIP-BE</setSpec>
</header>
<metadata><dc>
<publisher>HAL CCSD</publisher>
<title lang=en>Expression of E. coli RecA targeted to mitochondria of human cells.</title>
<creator>Paul, P</creator>
<creator>Dalibart, R</creator>
<creator>Lemoine, Soazig</creator>
<creator>Lestienne, P</creator>
<contributor>Université des Antilles (Pôle Guadeloupe) ; Université des Antilles (UA)</contributor>
<description>International audience</description>
<source>ISSN: 0027-5107</source>
<source>Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis</source>
<publisher>Elsevier</publisher>
<identifier>hal-01680533</identifier>
<identifier>https://hal.univ-antilles.fr/hal-01680533</identifier>
<source>https://hal.univ-antilles.fr/hal-01680533</source>
<source>Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, Elsevier, 2001, pp.11-9</source>
<identifier>PUBMED : 11356332</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/11356332</relation>
<language>en</language>
<subject>[SDE.BE] Environmental Sciences/Biodiversity and Ecology</subject>
<subject>[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology</subject>
<subject>[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN]</subject>
<subject>[SDV.EE.IEO] Life Sciences [q-bio]/Ecology, environment/Symbiosis</subject>
<subject>[SDV.TOX.ECO] Life Sciences [q-bio]/Toxicology/Ecotoxicology</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Mitochondrial DNA integrity is ensured by several nuclear-encoded proteins in vertebrates, and a number of mtDNA alterations in human diseases, including deletions and duplications, have been suspected to result from errors in the mitochondrial recombination pathway. However, the presence of the latter system is still a matter of controversy as RecA proteins display various functions in vitro. In Escherichia coli, RecA plays a central role in homologous recombination by pairing and transferring a single strand to a homologous duplex DNA. To address indirectly the issue of a mitochondrial recombination pathway in vivo, we have constructed a chimeric gene containing an N terminal mitochondrial targeting sequence and the E. coli RecA gene. Cells were transfected by the recombinant plasmid, then tested for their mtDNA repair upon bleomycin treatment. We found an increased repair rate of the mitochondrial DNA in cells expressing RecA as compared to control cells. These results indicate that the transfected cells display an improved mtDNA repair replication pathway due to the exogenous RecA, likely in synergy with an endogenous rate-limiting mitochondrial recombination pathway.</description>
<date>2001-06-05</date>
</dc>
</metadata>
</record>
</GetRecord>
</OAI-PMH>