Evidence map›Paper›PMID 27302019›Full record

ArticleMolecular oncology2016

Global re-wiring of p53 transcription regulation by the hepatitis B virus X protein.

Cheryl Chan, Thomas Thurnherr, Jingbo Wang, Xavier Gallart-Palau, Siu Kwan Sze, Steve Rozen, Caroline G Lee

Open access · bronzeAbstract read
In one paragraph

Article in Molecular oncology, 2016. 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
0.9field-weighted citation impact, top 22% 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, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  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

7 authors at 3 institutions in 1 country.

Cheryl ChanDivision of Medical Sciences, Humphrey Oei Institute of Cancer Research, National Cancer Centre Singapore, Singapore 169610, Singapore; NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore 117456, Singapore.
Thomas ThurnherrNUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore 117456, Singapore; Duke-NUS Graduate Medical School, Singapore 169857, Singapore.
Jingbo WangDepartment of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Singapore.
Xavier Gallart-PalauSchool of Biological Sciences, Nanyang Technological University, Singapore 637551, Singapore.
Siu Kwan SzeSchool of Biological Sciences, Nanyang Technological University, Singapore 637551, Singapore.
Steve RozenDuke-NUS Graduate Medical School, Singapore 169857, Singapore.
Caroline G LeeDivision of Medical Sciences, Humphrey Oei Institute of Cancer Research, National Cancer Centre Singapore, Singapore 169610, Singapore; NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore 117456, Singapore; Duke-NUS Graduate Medical School, Singapore 169857, Singapore; Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Singapore. Electronic address: caroline_lee@nuhs.edu.sg.
National University of Singapore · SGNanyang Technological University · SGDuke-NUS Medical School · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe tumour suppressor p53 is a central player in transcription regulation and cell fate determination. By interacting with p53 and altering its sequence-specific binding to the response elements, the hepatitis B virus X protein (HBx) was reported to re-direct p53 regulation of some genes.

resultsCoupling massively parallel deep sequencing with p53 chromatin immunoprecipitation, we demonstrate that HBx modulates global p53 site selection and that this was strongly influenced by altered interaction with transcription co-factors/co-regulators as well as post-translational modifications. Specifically, HBx attenuated p53-TBP-RB1 transcription complex recruitment and interaction and this was associated with hyper-phosphorylation of p53 at serine 315 by HBx. Concurrently, HBx enhanced p53 DNA occupancy to other response elements either alone by displacing specific transcription factors such as CEBPB and NFkB1, or in complex with distinct interacting co-factors Sp1, JUN and E2F1. Importantly, re-wiring of p53 transcription regulation by HBx was linked to the deregulation of genes involved in cell proliferation and death, suggesting a role of HBx in errant cell fate determination mediated by altered p53 site selection of target genes.

conclusionsOur study thus presents first evidence of global modes of p53 transcription alteration by HBx and provides new insights to understand and potentially curtail the viral oncoprotein.

Indexed as

Gene Expression Regulation, NeoplasticTranscription, GeneticCell DeathCell ProliferationConserved SequenceDNAHep G2 CellsHumansModels, BiologicalPhosphorylationPhosphoserineProtein BindingResponse ElementsTrans-ActivatorsTranscription FactorsTumor Suppressor Protein p53DNAhepatitis B virus X proteinPhosphoserineTrans-ActivatorsTranscription FactorsTumor Suppressor Protein p53Viral Regulatory and Accessory ProteinsChIP-SeqHBxp53 serine 315P53 transcriptionPhosphorylation

Identifiers

PMID27302019
PMCPMC5423203
OpenAlexW2418106425

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.