Evidence map›Paper›PMID 28077648›Full record

ArticleJournal of virology2017

Human Papillomavirus 16 E6 Upregulates APOBEC3B via the TEAD Transcription Factor.

Seiichiro Mori, Takamasa Takeuchi, Yoshiyuki Ishii, Takashi Yugawa, Tohru Kiyono, Hiroshi Nishina, Iwao Kukimoto

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 73 citations in OpenAlex.

  1. Trial
  2. Journal of virology · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Untargeted Mutation Triggered by Ribonucleoside Embedded in DNA.International journal of molecular sciences · 2024
    Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Clinical Implications of APOBEC3-Mediated Mutagenesis in Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 3 institutions in 1 country.

Seiichiro MoriPathogen Genomics Center, National Institute of Infectious Diseases, Tokyo, Japan moris@nih.go.jp.
Takamasa TakeuchiPathogen Genomics Center, National Institute of Infectious Diseases, Tokyo, Japan.
Yoshiyuki IshiiPathogen Genomics Center, National Institute of Infectious Diseases, Tokyo, Japan.
Takashi YugawaDivision of Carcinogenesis and Cancer Prevention, National Cancer Center Research Institute, Tokyo, Japan.
Tohru KiyonoDivision of Carcinogenesis and Cancer Prevention, National Cancer Center Research Institute, Tokyo, Japan.
Hiroshi NishinaDepartment of Developmental and Regenerative Biology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Iwao KukimotoPathogen Genomics Center, National Institute of Infectious Diseases, Tokyo, Japan.
National Institute of Infectious Diseases · JPGenesis Research Institute · JPTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cytidine deaminase APOBEC3B (A3B) underlies the genetic heterogeneity of several human cancers, including cervical cancer, which is caused by human papillomavirus (HPV) infection. We previously identified a region within the A3B promoter that is activated by the viral protein HPV16 E6 in human keratinocytes. Here, we discovered three sites recognized by the TEAD family of transcription factors within this region of the A3B promoter. Reporter assays in HEK293 cells showed that exogenously expressed TEAD4 induced A3B promoter activation through binding to these sites. Normal immortalized human keratinocytes expressing E6 (NIKS-E6) displayed increased levels of TEAD1/4 protein compared to parental NIKS. A series of E6 mutants revealed that E6-mediated degradation of p53 was important for increasing TEAD4 levels. Knockdown of TEADs in NIKS-E6 significantly reduced A3B mRNA levels, whereas ectopic expression of TEAD4 in NIKS increased A3B mRNA levels. Finally, chromatin immunoprecipitation assays demonstrated increased levels of TEAD4 binding to the A3B promoter in NIKS-E6 compared to NIKS. Collectively, these results indicate that E6 induces upregulation of A3B through increased levels of TEADs, highlighting the importance of the TEAD-A3B axis in carcinogenesis.

Indexed as

Host-Pathogen InteractionsUp-RegulationCell LineChromatin ImmunoprecipitationCytidine DeaminaseDNA-Binding ProteinsEpithelial CellsGene ExpressionGene Knockdown TechniquesHuman papillomavirus 16HumansMinor Histocompatibility AntigensMuscle ProteinsNuclear ProteinsOncogene Proteins, ViralProteolysisAPOBEC3B protein, humanCytidine DeaminaseDNA-Binding ProteinsE6 protein, Human papillomavirus type 16Minor Histocompatibility AntigensMuscle ProteinsNuclear ProteinsOncogene Proteins, ViralRepressor ProteinsTEAD1 protein, humanTEAD4 protein, humanTEA Domain Transcription FactorsTranscription FactorsTumor Suppressor Protein p53APOBEC3BE6papillomavirusTEAD

Identifiers

PMID28077648
PMCPMC5331809
OpenAlexW2578831276

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.