Evidence map›Paper›PMID 27545325›Full record

ArticleNature communications2016

Positive feedback regulation of p53 transactivity by DNA damage-induced ISG15 modification.

Jong Ho Park, Seung Wook Yang, Jung Mi Park, Seung Hyeun Ka, Ji-Hoon Kim, Young-Yun Kong, Young Joo Jeon, Jae Hong Seol, Chin Ha Chung

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

68 citing papers in PubMed, 110 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Berberine inhibits ISG15 and pyroptosis to attenuate diabetic kidney disease inflammation and fibrosis.Apoptosis : an international journal on programmed cell death · 2026
    Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. ISGylation: is our genome yearning for such a modification?Acta biochimica et biophysica Sinica · 2025
    Review
  12. Article
  13. Article
  14. Molecular Interplay of ISG15/ISGylation in Neuropathologies.CNS & neurological disorders drug targets · 2025
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

8 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 1 country.

Jong Ho ParkSchool of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 08826, Korea.
Seung Wook YangSchool of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 08826, Korea.
Jung Mi ParkSchool of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 08826, Korea.
Seung Hyeun KaSchool of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 08826, Korea.
Ji-Hoon KimSchool of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 08826, Korea.
Young-Yun KongSchool of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 08826, Korea.
Young Joo JeonDepartment of Biochemistry, Institute of Medical Science, Chungnam National University School of Medicine, Daejon 34134, Korea.
Jae Hong SeolSchool of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 08826, Korea.
Chin Ha ChungSchool of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 08826, Korea.
Seoul National University · KRChungnam National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p53 plays a pivotal role in tumour suppression under stresses, such as DNA damage. ISG15 has been implicated in the control of tumorigenesis. Intriguingly, the expression of ISG15, UBE1L and UBCH8 is induced by DNA-damaging agents, such as ultraviolet and doxorubicin, which are known to induce p53. Here, we show that the genes encoding ISG15, UBE1L, UBCH8 and EFP, have the p53-responsive elements and their expression is induced in a p53-dependent fashion under DNA damage conditions. Furthermore, DNA damage induces ISG15 conjugation to p53 and this modification markedly enhances the binding of p53 to the promoters of its target genes (for example, CDKN1 and BAX) as well as of its own gene by promoting phosphorylation and acetylation, leading to suppression of cell growth and tumorigenesis. These findings establish a novel feedback circuit between p53 and ISG15-conjugating system for positive regulation of the tumour suppressive function of p53 under DNA damage conditions.

Indexed as

Acetylationbcl-2-Associated X ProteinCarcinogenesisCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p21CytokinesDNA DamageDoxorubicinHumansPhosphorylationPromoter Regions, GeneticTumor Suppressor Protein p53Ubiquitin-Activating EnzymesUbiquitin-Conjugating EnzymesUbiquitinsBAX protein, humanbcl-2-Associated X ProteinCyclin-Dependent Kinase Inhibitor p21CytokinesDoxorubicinISG15 protein, humanTP53 protein, humanTumor Suppressor Protein p53UBA7 protein, humanUBE2L6 protein, humanUbiquitin-Activating EnzymesUbiquitin-Conjugating EnzymesUbiquitins

Identifiers

PMID27545325
PMCPMC4996943
OpenAlexW2513714775

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.