Evidence map›Paper›PMID 30945125›Full record

ArticleVirologica Sinica2019

HPV18 Utilizes Two Alternative Branch Sites for E6*I Splicing to Produce E7 Protein.

Ayslan Castro Brant, Vladimir Majerciak, Miguel Angelo Martins Moreira, Zhi-Ming Zheng

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Virologica Sinica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Article
  2. Article
  3. Alternative splicing in the genome of HPV and its regulation.Frontiers in cellular and infection microbiology · 2024
    Review
  4. RNA therapy is shining for genetic diseases.Molecular therapy. Nucleic acids · 2023
    Article
  5. Review
  6. Article
  7. High-Risk Human Papillomavirus Oncogenic E6/E7 mRNAs Splicing Regulation.Frontiers in cellular and infection microbiology · 2022
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. 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

4 authors.

Ayslan Castro BrantTumor Virus RNA Biology Section, RNA Biology Laboratory, Center for Cancer Research, National Cancer Institute, NIH, Frederick, MD, 21702, USA.
Vladimir MajerciakTumor Virus RNA Biology Section, RNA Biology Laboratory, Center for Cancer Research, National Cancer Institute, NIH, Frederick, MD, 21702, USA.
Miguel Angelo Martins MoreiraGenetics Program, Nacional Cancer Institute, INCA, Rio de Janeiro, 20231-050, Brazil.
Zhi-Ming ZhengTumor Virus RNA Biology Section, RNA Biology Laboratory, Center for Cancer Research, National Cancer Institute, NIH, Frederick, MD, 21702, USA. zhengt@exchange.nih.gov.ORCID http://orcid.org/0000-0001-5547-7912

Funding

Gene Expression and Post-Transcriptional Regulation of DNA Tumor VirusesZIASC010357 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI ZHENG, ZHI-MING · 2009 to 2025
$24.3M
Intramural NIH HHS ZIA SC010357
6 · The paper itself

Abstract

Human papillomavirus 18 (HPV18) E6 and E7 oncogenes are transcribed as a single bicistronic E6E7 pre-mRNA. The E6 ORF region in the bicistronic E6E7 pre-mRNA contains an intron. Splicing of this intron disrupts the E6 ORF integrity and produces a spliced E6*I RNA for efficient E7 translation. Here we report that the E6 intron has two overlapped branch point sequences (BPS) upstream of its 3' splice site, with an identical heptamer AACUAAC, for E6*I splicing. One heptamer has a branch site adenosine (underlined) at nt 384 and the other at nt 388. E6*I splicing efficiency correlates to the expression level of E6 and E7 proteins and depends on the selection of which branch site. In general, E6*I splicing prefers the 3'ss-proximal branch site at nt 388 over the distal branch site at nt 384. Inactivation of the nt 388 branch site was found to activate a cryptic acceptor site at nt 636 for aberrant RNA splicing. Together, these data suggest that HPV18 modulates its production ratio of E6 and E7 proteins by alternative selection of the two mapped branch sites for the E6*I splicing, which could be beneficial in its productive or oncogenic infection according to the host cell environment.

Indexed as

RNA SplicingDNA-Binding ProteinsHuman papillomavirus 18HumansIntronsOncogene Proteins, ViralRNA, MessengerRNA, ViralDNA-Binding ProteinsE6 protein, Human papillomavirus type 18E7 protein, Human papillomavirus type 18Oncogene Proteins, ViralRNA, MessengerRNA, ViralBranch pointE6, E7, E6 intronHPV oncogenesHPV splicingHuman papillomavirus 18 (HPV18)

Identifiers

PMID30945125
PMCPMC6513837

What OpenQuestion 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 OpenQuestion graph.