Evidence map›Paper›PMID 23967213›Full record

ArticlePloS one2013

The ING4 Binding with p53 and Induced p53 Acetylation were Attenuated by Human Papillomavirus 16 E6.

Yi Guo, Xiangkai Meng, Qian Wang, Yanan Wang, Hong Shang

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. INGs are potential drug targets for cancer.Journal of cancer research and clinical oncology · 2017
    Review
  8. The association of inhibitor of Growth 4 with its prognostic value in osteogenic sarcoma.International journal of clinical and experimental pathology · 2017
    Article
  9. Article
  10. Inhibitor of growth-4 is a potential target for cancer therapy.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  11. Article
  12. Article
  13. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Yi GuoDepartment of Gynecology, First Affiliated Hospital of China Medical University, Shenyang, China.
Xiangkai Meng
Qian Wang
Yanan Wang
Hong Shang
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High risk subtype HPV16 early oncoprotein E6 contributes host cell immortalization and transformation through interacting with a number of cellular factors. ING4 is one member of the inhibitor of growth (ING) family of type II tumor suppressors and it has been shown to be involved in regulating p53 function. However, the effect and mechanism of HPV16 E6 on ING4 function remain elusive. In this study, we report HPV16 E6 combines with ING4 in vivo and in vitro. The ING4 induced p53 acetylation and its combining with p53 were attenuated by HPV16 E6 independent of p53 degradation. The enhancing function of ING4 on p53 mediated apoptosis was diminished when HPV16 E6 existed. These findings reveal that ING4 may be a common target of oncogenic viruses for driving host cell carcinogenesis.

Indexed as

AcetylationApoptosisCell Cycle ProteinsCell Line, TumorCell Transformation, NeoplasticHomeodomain ProteinsHumansOncogene Proteins, ViralProtein BindingRepressor ProteinsTranscriptional ActivationTumor Suppressor Protein p53Tumor Suppressor ProteinsCell Cycle ProteinsE6 protein, Human papillomavirus type 16Homeodomain ProteinsING4 protein, humanOncogene Proteins, ViralRepressor ProteinsTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID23967213
PMCPMC3742747
OpenAlexW2060632473

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.