pubmed-article:10716434 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10716434 | lifeskim:mentions | umls-concept:C1167117 | lld:lifeskim |
pubmed-article:10716434 | pubmed:issue | 6773 | lld:pubmed |
pubmed-article:10716434 | pubmed:dateCreated | 2000-4-3 | lld:pubmed |
pubmed-article:10716434 | pubmed:abstractText | The bacterial SOS response to unusual levels of DNA damage has been recognized and studied for several decades. Pathways for re-establishing inactivated replication forks under normal growth conditions have received far less attention. In bacteria growing aerobically in the absence of SOS-inducing conditions, many replication forks encounter DNA damage, leading to inactivation. The pathways for fork reactivation involve the homologous recombination systems, are nonmutagenic, and integrate almost every aspect of DNA metabolism. On a frequency-of-use basis, these pathways represent the main function of bacterial DNA recombination systems, as well as the main function of a number of other enzymatic systems that are associated with replication and site-specific recombination. | lld:pubmed |
pubmed-article:10716434 | pubmed:language | eng | lld:pubmed |
pubmed-article:10716434 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10716434 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:10716434 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10716434 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10716434 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10716434 | pubmed:month | Mar | lld:pubmed |
pubmed-article:10716434 | pubmed:issn | 0028-0836 | lld:pubmed |
pubmed-article:10716434 | pubmed:author | pubmed-author:SherrattD JDJ | lld:pubmed |
pubmed-article:10716434 | pubmed:author | pubmed-author:MariansK JKJ | lld:pubmed |
pubmed-article:10716434 | pubmed:author | pubmed-author:KreuzerK NKN | lld:pubmed |
pubmed-article:10716434 | pubmed:author | pubmed-author:GoodmanM FMF | lld:pubmed |
pubmed-article:10716434 | pubmed:author | pubmed-author:SandlerS JSJ | lld:pubmed |
pubmed-article:10716434 | pubmed:author | pubmed-author:CoxM MMM | lld:pubmed |
pubmed-article:10716434 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10716434 | pubmed:day | 2 | lld:pubmed |
pubmed-article:10716434 | pubmed:volume | 404 | lld:pubmed |
pubmed-article:10716434 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10716434 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10716434 | pubmed:pagination | 37-41 | lld:pubmed |
pubmed-article:10716434 | pubmed:dateRevised | 2000-12-18 | lld:pubmed |
pubmed-article:10716434 | pubmed:meshHeading | pubmed-meshheading:10716434... | lld:pubmed |
pubmed-article:10716434 | pubmed:meshHeading | pubmed-meshheading:10716434... | lld:pubmed |
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pubmed-article:10716434 | pubmed:meshHeading | pubmed-meshheading:10716434... | lld:pubmed |
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pubmed-article:10716434 | pubmed:meshHeading | pubmed-meshheading:10716434... | lld:pubmed |
pubmed-article:10716434 | pubmed:year | 2000 | lld:pubmed |
pubmed-article:10716434 | pubmed:articleTitle | The importance of repairing stalled replication forks. | lld:pubmed |
pubmed-article:10716434 | pubmed:affiliation | Department of Biochemistry, University of Wisconsin-Madison, 53706-1544, USA. | lld:pubmed |
pubmed-article:10716434 | pubmed:publicationType | Journal Article | lld:pubmed |
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