| pubmed-article:9560379 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9560379 | lifeskim:mentions | umls-concept:C0014834 | lld:lifeskim |
| pubmed-article:9560379 | lifeskim:mentions | umls-concept:C0079866 | lld:lifeskim |
| pubmed-article:9560379 | lifeskim:mentions | umls-concept:C0037703 | lld:lifeskim |
| pubmed-article:9560379 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:9560379 | pubmed:dateCreated | 1998-6-26 | lld:pubmed |
| pubmed-article:9560379 | pubmed:abstractText | The cellular response to DNA damage that has been most extensively studied is the SOS response of Escherichia coli. Analyses of the SOS response have led to new insights into the transcriptional and post-translational regulation of processes that increase cell survival after DNA damage as well as insights into DNA-damage-induced mutagenesis, i.e., SOS mutagenesis. SOS mutagenesis requires the recA and umuDC gene products and has as its mechanistic basis the alteration of DNA polymerase III such that it becomes capable of replicating DNA containing miscoding and noncoding lesions. Ongoing investigations of the mechanisms underlying SOS mutagenesis, as well as recent observations suggesting that the umuDC operon may have a role in the regulation of the E. coli cell cycle after DNA damage has occurred, are discussed. | lld:pubmed |
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| pubmed-article:9560379 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9560379 | pubmed:citationSubset | IM | lld:pubmed |
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