Evidence map›Paper›PMID 32992873›Full record

ArticlePathogens (Basel, Switzerland)2020

The SMC5/6 Complex Represses the Replicative Program of High-Risk Human Papillomavirus Type 31.

Ryan T Gibson, Elliot J Androphy

Open access · goldAbstract read
In one paragraph

Article in Pathogens (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.6field-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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Chromatin Control of EBV Infection and Latency.Current topics in microbiology and immunology · 2025
    Article
  3. Article
  4. Review
  5. Regulation of R-Loops in DNA Tumor Viruses.Pathogens (Basel, Switzerland) · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Genome control by SMC complexes.Nature reviews. Molecular cell biology · 2023
    Review
  10. SMC-based immunity against extrachromosomal DNA elements.Biochemical Society transactions · 2023
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Smc5/6 silences episomal transcription by a three-step function.Nature structural & molecular biology · 2022
    Article
  17. Article
  18. Article
  19. Article
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.

Ryan T GibsonDepartment of Microbiology and Immunology, School of Medicine, Indiana University, Indianapolis, IN 46202, USA.
Elliot J AndrophyDepartment of Microbiology and Immunology, School of Medicine, Indiana University, Indianapolis, IN 46202, USA.ORCID 0000-0002-8104-0703
Indiana University – Purdue University Indianapolis · US

Funding

CONTROL OF PAPILLOMAVIRUS EXPRESSION AND TRANSFORMATIONR01CA058376 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI ANDROPHY, ELLIOT J. · 1993 to 2019
$5.7M
NCI/NIH CA058376NCI NIH HHS R01 CA058376
6 · The paper itself

Abstract

The multi-subunit structural maintenance of chromosomes (SMC) 5/6 complex includes SMC6 and non-SMC element (NSE)3. SMC5/6 is essential for homologous recombination DNA repair and functions as an antiviral factor during hepatitis B (HBV) and herpes simplex-1 (HSV-1) viral infections. Intriguingly, SMC5/6 has been found to associate with high-risk human papillomavirus (HPV) E2 regulatory proteins, but the functions of this interaction and its role during HPV infection remain unclear. Here, we further characterize SMC5/6 interactions with HPV-31 E2 and its role in the HPV life cycle. Co-immunoprecipitation (co-IP) revealed that SMC6 interactions with HPV-31 E2 require the E2 transactivation domain, implying that SMC5/6 interacts with full-length E2. Using chromatin immunoprecipitation, we found that SMC6 is present on HPV-31 episomes at E2 binding sites. Th depletion of SMC6 and NSE3 increased viral replication and transcription in keratinocytes maintaining episomal HPV-31, indicating that SMC5/6 restricts the viral replicative program. SMC6 interactions with E2 were reduced in the presence of HPV-31 E1, suggesting that SMC6 and E1 compete for E2 binding. Our findings demonstrate SMC5/6 functions as a repressor of the viral replicative program and this may involve inhibiting the initiation of viral replication.

Indexed as

E2NSE3papillomavirusreplicationSMC5/6structural maintenance of chromosomestranscription

Identifiers

PMID32992873
PMCPMC7599729
OpenAlexW3089199980

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.