ArticleThe Journal of general virology2008
Mutagenesis of the murine cytomegalovirus M56 terminase gene.
Article in The Journal of general virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- The human cytomegalovirus decathlon: Ten critical replication events provide opportunities for restriction.Frontiers in cell and developmental biology · 2022Review
- Mutual Interplay between the Human Cytomegalovirus Terminase Subunits pUL51, pUL56, and pUL89 Promotes Terminase Complex Formation.Journal of virology · 2017Article
- Vaccination with a Live Attenuated Cytomegalovirus Devoid of a Protein Kinase R Inhibitory Gene Results in Reduced Maternal Viremia and Improved Pregnancy Outcome in a Guinea Pig Congenital Infection Model.Journal of virology · 2015Article
- Neutralizing activity of saliva against cytomegalovirus.Clinical and vaccine immunology : CVI · 2011Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The murine cytomegalovirus (MCMV) M56 is one of three proteins that combine to form the MCMV terminase, required for cleavage and packaging of viral DNA into capsids. Deletion of M56 from a bacterial artificial chromosome (BAC) clone of the MCMV genome was considered lethal, as the mutant BAC failed to reconstitute infectious virus. Reintroduction of M56 at an ectopic locus complemented the deletion, allowing reconstitution of a virus that replicated with wild-type efficiency. However, neither the reintroduction of M56 sequences encoding an N-terminal epitope fusion nor a mutation targeting a region in M56 implicated as an ATPase active site was capable of restoring virus viability. In contrast, a frame shift mutation in M56a, a putative open reading frame that overlaps M56, had no effect on viral replication. We conclude that M56a is dispensable, whereas M56 residues comprising the proposed ATPase active site are critical for terminase function and viral replication.
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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.