| pubmed-article:14616075 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14616075 | lifeskim:mentions | umls-concept:C2004454 | lld:lifeskim |
| pubmed-article:14616075 | lifeskim:mentions | umls-concept:C0237477 | lld:lifeskim |
| pubmed-article:14616075 | lifeskim:mentions | umls-concept:C0598316 | lld:lifeskim |
| pubmed-article:14616075 | pubmed:dateCreated | 2003-11-17 | lld:pubmed |
| pubmed-article:14616075 | pubmed:abstractText | DNA damage encountered during the cellular process of chromosomal replication can disrupt the replication machinery and result in mutagenesis or lethality. The RecA protein of Escherichia coli is essential for survival in this situation: It maintains the integrity of the arrested replication fork and signals the upregulation of over 40 gene products, of which most are required to restore the genomic template and to facilitate the resumption of processive replication. Although RecA was originally discovered as a gene product that was required to change the genetic information during sexual cell cycles, over three decades of research have revealed that it is also the key enzyme required to maintain the genetic information when DNA damage is encountered during replication in asexual cell cycles. In this review, we examine the significant experimental approaches that have led to our current understanding of the RecA-mediated processes that restore replication following encounters with DNA damage. | lld:pubmed |
| pubmed-article:14616075 | pubmed:language | eng | lld:pubmed |
| pubmed-article:14616075 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14616075 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:14616075 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14616075 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14616075 | pubmed:issn | 0066-4197 | lld:pubmed |
| pubmed-article:14616075 | pubmed:author | pubmed-author:HanawaltPhili... | lld:pubmed |
| pubmed-article:14616075 | pubmed:author | pubmed-author:CourcelleJust... | lld:pubmed |
| pubmed-article:14616075 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:14616075 | pubmed:volume | 37 | lld:pubmed |
| pubmed-article:14616075 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:14616075 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:14616075 | pubmed:pagination | 611-46 | lld:pubmed |
| pubmed-article:14616075 | pubmed:dateRevised | 2005-11-16 | lld:pubmed |
| pubmed-article:14616075 | pubmed:meshHeading | pubmed-meshheading:14616075... | lld:pubmed |
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| pubmed-article:14616075 | pubmed:meshHeading | pubmed-meshheading:14616075... | lld:pubmed |
| pubmed-article:14616075 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:14616075 | pubmed:articleTitle | RecA-dependent recovery of arrested DNA replication forks. | lld:pubmed |
| pubmed-article:14616075 | pubmed:affiliation | Department of Biological Sciences, Box GY, Mississippi State University, Mississippi State, Mississippi 39762, USA. jcourcelle@biology.msstate.edu | lld:pubmed |
| pubmed-article:14616075 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:14616075 | pubmed:publicationType | Review | lld:pubmed |
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