ArticleJournal of virology2019
Contribution of DNA Replication to the FAM111A-Mediated Simian Virus 40 Host Range Phenotype.
Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 citations in OpenAlex.
- Expanding TBCE-related phenotype-novel variant causing rigid spine, eosinophilia, neutropenia, and nocturnal hypoxemia.Journal of applied genetics · 2025Pooled it
- Expanding the Phenotypic Spectrum of Kenny-Caffey Syndrome.The Journal of clinical endocrinology and metabolism · 2023Pooled it
- The FAM111A Gene: Genetic, Epigenetic, and Pharmacological Targets and Mechanistic Insights with Clinical Relevance.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Quantitative hypermorphic FAM111A alleles cause autosomal recessive Kenny-Caffey syndrome type 2 and osteocraniostenosis.JCI insight · 2025Article
- Regulation of viral replication by host restriction factors.Frontiers in immunology · 2025Review
- E2F3-dependent activation of FAM111B restricts mouse cytomegalovirus replication in primate cells.Journal of virology · 2024Article
- Dimerization-dependent serine protease activity of FAM111A prevents replication fork stalling at topoisomerase 1 cleavage complexes.Nature communications · 2024Article
- Unravelling the Intricate Roles of FAM111A and FAM111B: From Protease-Mediated Cellular Processes to Disease Implications.International journal of molecular sciences · 2024Review
- FAM111A regulates replication origin activation and cell fitness.Life science alliance · 2023Article
- Human FAM111A inhibits vaccinia virus replication by degrading viral protein I3 and is antagonized by poxvirus host range factor SPI-1.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Gene-nutrient interactions that impact magnesium homeostasis increase risk for neural tube defects in mice exposed to dolutegravir.Frontiers in cell and developmental biology · 2023Article
- FAM111A is dispensable for electrolyte homeostasis in mice.Scientific reports · 2022Article
- Functions and evolution of FAM111 serine proteases.Frontiers in molecular biosciences · 2022Review
- Differential Regulation of Cellular FAM111B by Human Adenovirus C Type 5 E1 Oncogenes.Viruses · 2021Article
- Exploration of binary protein-protein interactions between tick-borne flaviviruses and Ixodes ricinus.Parasites & vectors · 2021Article
- FAM111A induces nuclear dysfunction in disease and viral restriction.EMBO reports · 2021Article
- FAM111 protease activity undermines cellular fitness and is amplified by gain-of-function mutations in human disease.EMBO reports · 2020Article
- FAM111A protects replication forks from protein obstacles via its trypsin-like domain.Nature communications · 2020Article
- Molecular and Clinical Characterization of a Novel Prognostic and Immunologic Biomarker FAM111A in Diffuse Lower-Grade Glioma.Frontiers in oncology · 2020Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Host range (HR) mutants of simian virus 40 (SV40) containing mutations in the C terminus of large T antigen fail to replicate efficiently or form plaques in restrictive cell types. HR mutant viruses exhibit impairments at several stages of the viral life cycle, including early and late gene and protein expression, DNA replication, and virion assembly, although the underlying mechanism for these defects is unknown. Host protein FAM111A, whose depletion rescues early and late gene expression and plaque formation for SV40 HR viruses, has been shown to play a role in cellular DNA replication. SV40 viral DNA replication occurs in the nucleus of infected cells in viral replication centers where viral proteins and cellular replication factors localize. Here, we examined the role of viral replication center formation and DNA replication in the FAM111A-mediated HR phenotype. We found that SV40 HR virus rarely formed viral replication centers in restrictive cells, a phenotype that could be rescued by FAM111A depletion. Furthermore, while FAM111A localized to nucleoli in uninfected cells in a cell cycle-dependent manner, FAM111A relocalized to viral replication centers after infection with SV40 wild-type or HR viruses. We also found that inhibition of viral DNA replication through aphidicolin treatment or through the use of replication-defective SV40 mutants diminished the effects of FAM111A depletion on viral gene expression. These results indicate that FAM111A restricts SV40 HR viral replication center formation and that viral DNA replication contributes to the FAM111A-mediated effect on early gene expression.
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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.