ArticleJournal of virology2000
Two widely spaced initiator binding sites create an HMG1-dependent parvovirus rolling-hairpin replication origin.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Article
- Twenty years of human bocavirus research: from an unculturable virus of unclear pathogenicity to a culturable human pathogen and gene therapy vector candidate.Clinical microbiology reviews · 2025Review
- Recent Advances in Molecular Biology of Human Bocavirus 1 and Its Applications.Frontiers in microbiology · 2021Review
- Mutations in the C-terminus of HBoV NS1 affect the function of NP1.Scientific reports · 2017Article
- Analysis of cis and trans Requirements for DNA Replication at the Right-End Hairpin of the Human Bocavirus 1 Genome.Journal of virology · 2016Article
- Circulating HMGB1 and RAGE as Clinical Biomarkers in Malignant and Autoimmune Diseases.Diagnostics (Basel, Switzerland) · 2015Review
- Structures of minute virus of mice replication initiator protein N-terminal domain: Insights into DNA nicking and origin binding.Virology · 2015Article
- Tumor Selectivity of Oncolytic Parvoviruses: From in vitro and Animal Models to Cancer Patients.Frontiers in bioengineering and biotechnology · 2015Review
- Complementary induction of immunogenic cell death by oncolytic parvovirus H-1PV and gemcitabine in pancreatic cancer.Journal of virology · 2014Article
- Article
- Article
- The genome of human parvovirus b19 can replicate in nonpermissive cells with the help of adenovirus genes and produces infectious virus.Journal of virology · 2009Article
- Human HMGB1 directly facilitates interactions between nucleotide excision repair proteins on triplex-directed psoralen interstrand crosslinks.DNA repair · 2009Article
- Replication initiator protein NS1 of the parvovirus minute virus of mice binds to modular divergent sites distributed throughout duplex viral DNA.Journal of virology · 2007Article
- Segregation of a single outboard left-end origin is essential for the viability of parvovirus minute virus of mice.Journal of virology · 2006Article
- Possible active origin of replication in the double stranded extended form of the left terminus of LuIII and its implication on the replication model of the parvovirus.Virology journal · 2005Article
- Genome packaging sense is controlled by the efficiency of the nick site in the right-end replication origin of parvoviruses minute virus of mice and LuIII.Journal of virology · 2005Article
- Bidirectional replication from an internal ori site of the linear N15 plasmid prophage.Nucleic acids research · 2003Article
- Construction and production of oncotropic vectors, derived from MVM(p), that share reduced sequence homology with helper plasmids.Cancer gene therapy · 2002Article
- Minute virus of mice initiator protein NS1 and a host KDWK family transcription factor must form a precise ternary complex with origin DNA for nicking to occur.Journal of virology · 2001Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Minute virus of mice (MVM) replicates via a linearized form of rolling-circle replication in which the viral nickase, NS1, initiates DNA synthesis by introducing a site-specific nick into either of two distinct origin sequences. In vitro nicking and replication assays with substrates that had deletions or mutations were used to explore the sequences and structural elements essential for activity of one of these origins, located in the right-end (5') viral telomere. This structure contains 248 nucleotides, most-favorably arranged as a simple hairpin with six unpaired bases. However, a pair of opposing NS1 binding sites, located near its outboard end, create a 33-bp palindrome that could potentially assume an alternate cruciform configuration and hence directly bind HMG1, the essential cofactor for this origin. The palindromic nature of this sequence, and thus its ability to fold into a cruciform, was dispensable for origin function, as was the NS1 binding site occupying the inboard arm of the palindrome. In contrast, the NS1 site in the outboard arm was essential for initiation, even though positioned 120 bp from the nick site. The specific sequence of the nick site and an additional NS1 binding site which directly orients NS1 over the initiation site were also essential and delimited the inboard border of the minimal right-end origin. DNase I and hydroxyl radical footprints defined sequences protected by NS1 and suggest that HMG1 allows the NS1 molecules positioned at each end of the origin to interact, creating a distortion characteristic of a double helical loop.
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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.