Evidence map›Paper›PMID 26882543›Full record

ArticleEMBO reports2016

NAT10 regulates p53 activation through acetylating p53 at K120 and ubiquitinating Mdm2.

Xiaofeng Liu, Yuqin Tan, Chunfeng Zhang, Ying Zhang, Liangliang Zhang, Pengwei Ren, Hongkui Deng, Jianyuan Luo, Yang Ke, Xiaojuan Du

Open access · greenAbstract read
In one paragraph

Article in EMBO reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing 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

137 citing papers in PubMed, 223 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. NAT10-Mediated ac4C Modification of circANKRD12 Reprograms the Tumor Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  6. Review
  7. Article
  8. The NAT10/c-Myc positive feedback loop orchestrates tRNA acCellular & molecular biology letters · 2026
    Article
  9. Article
  10. Article
  11. NAT10/acProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. The NAT10/acCell communication and signaling : CCS · 2026
    Review
  18. Review
  19. Cancer Stem Cells Shift Metabolite Acetyl-Coenzyme A to Abrogate the Differentiation of CD103Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  20. Article

77 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

10 authors at 3 institutions in 2 countries.

Xiaofeng LiuKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Health Science Center, Beijing, China Department of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Yuqin TanKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Health Science Center, Beijing, China Department of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Chunfeng ZhangKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Health Science Center, Beijing, China Department of Medical Genetics, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Ying ZhangKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Health Science Center, Beijing, China Laboratory of Genetics, Peking University School of Oncology, Peking University Cancer Hospital & Institute, Beijing, China.
Liangliang ZhangKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Health Science Center, Beijing, China Department of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Pengwei RenKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Health Science Center, Beijing, China Department of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Hongkui DengKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Health Science Center, Beijing, China Department of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Jianyuan LuoKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Health Science Center, Beijing, China Department of Medical Genetics, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China Department of Medical & Research Technology, School of Medicine, University of Maryland, Baltimore, MD, USA.
Yang KeKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Health Science Center, Beijing, China Laboratory of Genetics, Peking University School of Oncology, Peking University Cancer Hospital & Institute, Beijing, China.
Xiaojuan DuKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Health Science Center, Beijing, China Department of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China duxiaojuan100@bjmu.edu.cn.
Peking University · CNPeking University Cancer Hospital · CNUniversity of Maryland, Baltimore · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As a genome guardian, p53 maintains genome stability by arresting cells for damage repair or inducing cell apoptosis to eliminate the damaged cells in stress response. Several nucleolar proteins stabilize p53 by interfering Mdm2-p53 interaction upon cellular stress, while other mechanisms by which nucleolar proteins activate p53 remain to be determined. Here, we identify NAT10 as a novel regulator for p53 activation. NAT10 acetylates p53 at K120 and stabilizes p53 by counteracting Mdm2 action. In addition, NAT10 promotes Mdm2 degradation with its intrinsic E3 ligase activity. After DNA damage, NAT10 translocates to nucleoplasm and activates p53-mediated cell cycle control and apoptosis. Finally, NAT10 inhibits cell proliferation and expression of NAT10 decreases in human colorectal carcinomas. Thus, our data demonstrate that NAT10 plays a critical role in p53 activation via acetylating p53 and counteracting Mdm2 action, providing a novel pathway by which nucleolar protein activates p53 as a cellular stress sensor.

Indexed as

UbiquitinationAcetylationActive Transport, Cell NucleusApoptosisCell NucleusColorectal NeoplasmsDNA DamageHCT116 CellsHEK293 CellsHumansN-Terminal Acetyltransferase EN-Terminal AcetyltransferasesProtein BindingProtein StabilityProteolysisProto-Oncogene Proteins c-mdm2MDM2 protein, humanNAT10 protein, humanN-Terminal Acetyltransferase EN-Terminal AcetyltransferasesProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53acetylationE3 ligaseMdm2NAT10p53

Identifiers

PMID26882543
PMCPMC4772976
OpenAlexW2291365506

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.