| pubmed-article:8011018 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8011018 | lifeskim:mentions | umls-concept:C0014834 | lld:lifeskim |
| pubmed-article:8011018 | lifeskim:mentions | umls-concept:C0205160 | lld:lifeskim |
| pubmed-article:8011018 | lifeskim:mentions | umls-concept:C1155650 | lld:lifeskim |
| pubmed-article:8011018 | lifeskim:mentions | umls-concept:C1709060 | lld:lifeskim |
| pubmed-article:8011018 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:8011018 | pubmed:dateCreated | 1994-6-14 | lld:pubmed |
| pubmed-article:8011018 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8011018 | pubmed:abstractText | In E. coli, replication initiates at a genetically unique origin, oriC. Rapidly growing cells contain multiple oriC copies. Initiation occurs synchronously, once and only once per cell cycle at all origins present. Secondary initiations are prevented by a sequestration process that acts uniquely on newly replicated origins, which are marked because they are hemimethylated at GATC sites. We report the identification of a gene required for sequestration and demonstrate that this gene, seqA, also serves as a negative modulator of the primary initiation process. All previously identified in vivo initiation factors play positive roles. Thus, precise control of replication initiation may involve a balance between positive and negative elements. We suggest that SeqA might be a cooperativity factor, acting to make the replication initiation process dependent upon cooperative interactions among components. | lld:pubmed |
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| pubmed-article:8011018 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:8011018 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8011018 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8011018 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8011018 | pubmed:month | May | lld:pubmed |
| pubmed-article:8011018 | pubmed:issn | 0092-8674 | lld:pubmed |
| pubmed-article:8011018 | pubmed:author | pubmed-author:BoydDD | lld:pubmed |
| pubmed-article:8011018 | pubmed:author | pubmed-author:LuMM | lld:pubmed |
| pubmed-article:8011018 | pubmed:author | pubmed-author:KlecknerNN | lld:pubmed |
| pubmed-article:8011018 | pubmed:author | pubmed-author:CampbellJ LJL | lld:pubmed |
| pubmed-article:8011018 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8011018 | pubmed:day | 6 | lld:pubmed |
| pubmed-article:8011018 | pubmed:volume | 77 | lld:pubmed |
| pubmed-article:8011018 | pubmed:geneSymbol | dnaA | lld:pubmed |
| pubmed-article:8011018 | pubmed:geneSymbol | seqA | lld:pubmed |
| pubmed-article:8011018 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8011018 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8011018 | pubmed:pagination | 413-26 | lld:pubmed |
| pubmed-article:8011018 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:8011018 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:8011018 | pubmed:articleTitle | SeqA: a negative modulator of replication initiation in E. coli. | lld:pubmed |
| pubmed-article:8011018 | pubmed:affiliation | Department of Biochemistry and Molecular Biology Harvard University, Cambridge, Massachusetts 02138. | lld:pubmed |
| pubmed-article:8011018 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8011018 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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