Evidence map›Paper›PMID 14747526›Full record

ArticleJournal of virology2004

Recruitment of replication protein A by the papillomavirus E1 protein and modulation by single-stranded DNA.

Yueh-Ming Loo, Thomas Melendy

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

61 citing papers in PubMed, 109 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Role of HPV16 E1 in cervical carcinogenesis.Frontiers in cellular and infection microbiology · 2022
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Human Papillomavirus Type 16International journal of medical sciences · 2019
    Article
  18. Article
  19. Article
  20. Article

1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Yueh-Ming LooDepartment of Microbiology, and Witebsky Center for Microbial Pathogenesis and Immunology, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, New York 14214, USA.
Thomas Melendy
University at Buffalo, State University of New York · US

Funding

HPV DNA REPLICATION: NOVEL HOST FACTORSK02AI001686 · NIAID · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI MELENDY, THOMAS · 1999 to 2003
$421k
PAPILLOMAVIRUS DNA REPLICATION--HOST CELL FACTORSR29GM056406 · NIGMS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI MELENDY, THOMAS · 1997 to 2001
$226k
NIAID NIH HHS AI01686NIGMS NIH HHS GM56406NIGMS NIH HHS R29 GM056406
6 · The paper itself

Abstract

With the exception of viral proteins E1 and E2, papillomaviruses depend heavily on host replication machinery for replication of their viral genome. E1 and E2 are known to recruit many of the necessary cellular replication factors to the viral origin of replication. Previously, we reported a physical interaction between E1 and the major human single-stranded DNA (ssDNA)-binding protein, replication protein A (RPA). E1 was determined to bind to the 70-kDa subunit of RPA, RPA70. In this study, using E1-affinity coprecipitation and enzyme-linked immunosorbent assay-based interaction assays, we show that E1 interacts with the major ssDNA-binding domain of RPA. Consistent with our previous report, no measurable interaction between E1 and the two smaller subunits of RPA was detected. The interaction of E1 with RPA was substantially inhibited by ssDNA. The extent of this inhibition was dependent on the length of the DNA. A 31-nucleotide (nt) oligonucleotide strongly inhibited the E1-RPA interaction, while a 16-nt oligonucleotide showed an intermediate level of inhibition. In contrast, a 10-nt oligonucleotide showed no observable effect on the E1-RPA interaction. This inhibition was not dependent on the sequence of the DNA. Furthermore, ssDNA also inhibited the interaction of RPA with papillomavirus E2, simian virus 40 T antigen, human polymerase alpha-primase, and p53. Taken together, our results suggest a potential role for ssDNA in modulating RPA-protein interactions, in particular, the RPA-E1 interactions during papillomavirus DNA replication. A model for recruitment of RPA by E1 during papillomavirus DNA replication is proposed.

Indexed as

DNA ReplicationPapillomaviridaeBinding, CompetitiveChemical PrecipitationDNA-Binding ProteinsDNA, Single-StrandedEnzyme-Linked Immunosorbent AssayHumansOligonucleotidesReplication Protein AViral ProteinsDNA-Binding ProteinsDNA, Single-StrandedE1 protein, Human papillomavirus type 11OligonucleotidesReplication Protein ARPA1 protein, humanViral Proteins

Identifiers

PMID14747526
PMCPMC369418
OpenAlexW2157299442

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.