ArticlemBio2011
Functional reorganization of promyelocytic leukemia nuclear bodies during BK virus infection.
Article in mBio, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 44 citations in OpenAlex.
- Analysis of Several Common APOBEC-type Mutations in Bladder Tumors Suggests Links to Viral Infection.Cancer prevention research (Philadelphia, Pa.) · 2023Article
- Article
- Single-Cell, High-Content Microscopy Analysis of BK Polyomavirus Infection.Microbiology spectrum · 2023Article
- The interactions between PML nuclear bodies and small and medium size DNA viruses.Virology journal · 2023Review
- Replication Compartments of Eukaryotic and Bacterial DNA Viruses: Common Themes Between Different Domains of Host Cells.Annual review of virology · 2022Review
- BK Polyomavirus Requires the Mismatch Repair Pathway for DNA Damage Response Activation.Journal of virology · 2022Article
- Dual signaling via interferon and DNA damage response elicits entrapment by giant PML nuclear bodies.eLife · 2022Article
- A Cell Culture Model of BK Polyomavirus Persistence, Genome Recombination, and Reactivation.mBio · 2021Article
- Review
- Polyomavirus T Antigen InducesmBio · 2019Article
- Human polyomavirus BKV infection of endothelial cells results in interferon pathway induction and persistence.PLoS pathogens · 2019Article
- Biology of the BKPyV: An Update.Viruses · 2017Review
- The Role of Nuclear Antiviral Factors against Invading DNA Viruses: The Immediate Fate of Incoming Viral Genomes.Viruses · 2016Review
- Functional Upregulation of the DNA Cytosine Deaminase APOBEC3B by Polyomaviruses.Journal of virology · 2016Article
- Article
- Emerging Role of PML Nuclear Bodies in Innate Immune Signaling.Journal of virology · 2016Review
- Quantitative Proteomic Analysis of Enriched Nuclear Fractions from BK Polyomavirus-Infected Primary Renal Proximal Tubule Epithelial Cells.Journal of proteome research · 2015Article
- Viral DNA replication-dependent DNA damage response activation during BK polyomavirus infection.Journal of virology · 2015Article
- Crystal structure of cytomegalovirus IE1 protein reveals targeting of TRIM family member PML via coiled-coil interactions.PLoS pathogens · 2014Article
- JC virus inclusions in progressive multifocal leukoencephalopathy: scaffolding promyelocytic leukemia nuclear bodies grow with cell cycle transition through an S-to-G2-like state in enlarging oligodendrocyte nuclei.Journal of neuropathology and experimental neurology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
BK virus (BKV) is the causative agent for polyomavirus-associated nephropathy, a severe disease found in renal transplant patients due to reactivation of a persistent BKV infection. BKV replication relies on the interactions of BKV with many nuclear components, and subnuclear structures such as promyelocytic leukemia nuclear bodies (PML-NBs) are known to play regulatory roles during a number of DNA virus infections. In this study, we investigated the relationship between PML-NBs and BKV during infection of primary human renal proximal tubule epithelial (RPTE) cells. While the levels of the major PML-NB protein components remained unchanged, BKV infection of RPTE cells resulted in dramatic alterations in both the number and the size of PML-NBs. Furthermore, two normally constitutive components of PML-NBs, Sp100 and hDaxx, became dispersed from PML-NBs. To define the viral factors responsible for this reorganization, we examined the cellular localization of the BKV large tumor antigen (TAg) and viral DNA. TAg colocalized with PML-NBs during early infection, while a number of BKV chromosomes were adjacent to PML-NBs during late infection. We demonstrated that TAg alone was not sufficient to reorganize PML-NBs and that active viral DNA replication is required. Knockdown of PML protein did not dramatically affect BKV growth in culture. BKV infection, however, was able to rescue the growth of an ICP0-null herpes simplex virus 1 mutant whose growth defect was partially due to its inability to disrupt PML-NBs. We hypothesize that the antiviral functions of PML-NBs are inactivated through reorganization during normal BKV infection.
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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.