| pubmed-article:10778854 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10778854 | lifeskim:mentions | umls-concept:C1167117 | lld:lifeskim |
| pubmed-article:10778854 | lifeskim:mentions | umls-concept:C0035681 | lld:lifeskim |
| pubmed-article:10778854 | lifeskim:mentions | umls-concept:C0449258 | lld:lifeskim |
| pubmed-article:10778854 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
| pubmed-article:10778854 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:10778854 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:10778854 | pubmed:dateCreated | 2000-5-22 | lld:pubmed |
| pubmed-article:10778854 | pubmed:abstractText | We have discovered a correlation between the ability of Escherichia coli cells to survive damage to DNA and their ability to modulate RNA polymerase via the stringent response regulators, (p)ppGpp. Elevation of (p)ppGpp, or certain mutations in the beta subunit of RNA polymerase, dramatically improve survival of UV-irradiated strains lacking the RuvABC Holliday junction resolvase. Increased survival depends on excision and recombination proteins and relies on the ability of RecG helicase to form Holliday junctions from replication forks stalled at lesions in the DNA and of PriA to initiate replication restart. The role of RecG provides novel insights into the interplay between transcription, replication, and recombination, and suggests a general model in which recombination underpins genome duplication in the face of frequent obstacles to replication fork progression. | lld:pubmed |
| pubmed-article:10778854 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:10778854 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10778854 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10778854 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:10778854 | pubmed:issn | 0092-8674 | lld:pubmed |
| pubmed-article:10778854 | pubmed:author | pubmed-author:LloydR GRG | lld:pubmed |
| pubmed-article:10778854 | pubmed:author | pubmed-author:McGlynnPP | lld:pubmed |
| pubmed-article:10778854 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10778854 | pubmed:day | 31 | lld:pubmed |
| pubmed-article:10778854 | pubmed:volume | 101 | lld:pubmed |
| pubmed-article:10778854 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10778854 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10778854 | pubmed:pagination | 35-45 | lld:pubmed |
| pubmed-article:10778854 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:10778854 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10778854 | pubmed:articleTitle | Modulation of RNA polymerase by (p)ppGpp reveals a RecG-dependent mechanism for replication fork progression. | lld:pubmed |
| pubmed-article:10778854 | pubmed:affiliation | Institute of Genetics, University of Nottingham, Queen's Medical Centre, United Kingdom. | lld:pubmed |
| pubmed-article:10778854 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10778854 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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