ArticlePlasmid2012
Structure-function analysis of the SaPIbov1 replication origin in Staphylococcus aureus.
Article in Plasmid, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- SV40 T-antigen uses a DNA shearing mechanism to initiate origin unwinding.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Staphylococcal self-loading helicases couple the staircase mechanism with inter domain high flexibility.Nucleic acids research · 2022Article
- Genome replication dynamics of a bacteriophage and its satellite reveal strategies for parasitism and viral restriction.Nucleic acids research · 2020Article
- Pathogenicity Islands and Their Role in Staphylococcal Biology.Microbiology spectrum · 2019Review
- Convergent evolution of pathogenicity islands in helper cos phage interference.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Article
- Staphylococcal SCCmec elements encode an active MCM-like helicase and thus may be replicative.Nature structural & molecular biology · 2016Article
- Sequence determinants for DNA packaging specificity in the S. aureus pathogenicity island SaPI1.Plasmid · 2014Article
- Staphylococcal pathogenicity island interference with helper phage reproduction is a paradigm of molecular parasitism.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The SaPIs and their relatives are phage satellites and are unique among the known bacterial pathogenicity islands in their ability to replicate autonomously. They possess a phage-like replicon, which is organized as two sets of iterons arrayed symmetrically to flank an AT-rich region that is driven to melt by the binding of a SaPI-specific initiator (Rep) to the flanking iterons. Extensive deletion analysis has revealed that Rep can bind to a single iteron, generating a simple shift in a gel mobility assay; when bound on both sides, a second retarded band is seen, suggesting independent binding. Binding to both sites of the ori is necessary but not sufficient to melt the AT-rich region and initiate replication. For these processes, virtually the entire origin must be present. Since SaPI replication can be initiated on linear DNA, it is suggested that bilateral binding may be necessary to constrain the intervening DNA to enable Rep-driven melting.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.