ArticleVirology2011
Recruitment of DNA replication and damage response proteins to viral replication centers during infection with NS2 mutants of Minute Virus of Mice (MVM).
Article in Virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
39 citing papers in PubMed, 52 citations in OpenAlex.
- Delineated domain of VP2 capsid protein in H-1 parvovirus that determines susceptibility to human cancer cells.Journal of microbiology (Seoul, Korea) · 2026Article
- Adeno-Associated Virus 2 (AAV2) - Induced RPA exhaustion generates cellular DNA damage and restricts viral gene expression.PLoS pathogens · 2025Article
- Review
- Chaperonin TRiC/CCT subunit CCT7 is involved in the replication of canine parvovirus in F81 cells.Frontiers in microbiology · 2024Article
- For better or worse: crosstalk of parvovirus and host DNA damage response.Frontiers in immunology · 2024Review
- The DNA Damage Sensor MRE11 Regulates Efficient Replication of the Autonomous Parvovirus Minute Virus of Mice.Journal of virology · 2023Article
- The Autonomous Parvovirus Minute Virus of Mice Localizes to Cellular Sites of DNA Damage Using ATR Signaling.Viruses · 2023Article
- Genomes of the autonomous parvovirus minute virus of mice induce replication stress through RPA exhaustion.PLoS pathogens · 2023Article
- Nuclear entry and egress of parvoviruses.Molecular microbiology · 2022Review
- The small nonstructural protein NP1 of human bocavirus 1 directly interacts with Ku70 and RPA70 and facilitates viral DNA replication.PLoS pathogens · 2022Article
- Parvovirus nonstructural protein 2 interacts with chromatin-regulating cellular proteins.PLoS pathogens · 2022Article
- The adeno-associated virus 2 genome and Rep 68/78 proteins interact with cellular sites of DNA damage.Human molecular genetics · 2022Article
- The Large Nonstructural Protein (NS1) of Human Bocavirus 1 Directly Interacts with Ku70, Which Plays an Important Role in Virus Replication in Human Airway Epithelia.Journal of virology · 2022Article
- G2/M checkpoint regulation and apoptosis facilitate the nuclear egress of parvoviral capsids.Frontiers in cell and developmental biology · 2022Article
- Small but mighty: old and new parvoviruses of veterinary significance.Virology journal · 2021Review
- Concepts to Reveal Parvovirus-Nucleus Interactions.Viruses · 2021Review
- Article
- The NS1 protein of the parvovirus MVM Aids in the localization of the viral genome to cellular sites of DNA damage.PLoS pathogens · 2020Article
- Murine polyomavirus DNA transitions through spatially distinct nuclear replication subdomains during infection.PLoS pathogens · 2020Article
- Virus DNA Replication and the Host DNA Damage Response.Annual review of virology · 2018Review
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 1 institution in 1 country.
Funding
Abstract
MVM NS2 is essential for viral DNA amplification, but its mechanism of action is unknown. A classification scheme for autonomous parvovirus-associated replication (APAR) center development, based on NS1 distribution, was used to characterize abnormal APAR body maturation in NS2null mutant infections, and their organization examined for defects in host protein recruitment. Since acquisition of known replication factors appeared normal, we looked for differences in invoked DNA damage responses. We observed widespread association of H2AX/MDC1 damage response foci with viral replication centers, and sequestration and complex hyperphosphorylation of RPA(32), which occurred in wildtype and mutant infections. Quantifying these responses by western transfer indicated that both wildtype and NS2 mutant MVM elicited ATM activation, while phosphorylation of ATR, already basally activated in asynchronous A9 cells, was downregulated. We conclude that MVM infection invokes multiple damage responses that influence the APAR environment, but that NS2 does not modify the recruitment of cellular proteins.
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.