Evidence map›Paper›PMID 23677994›Full record

ArticleThe Journal of biological chemistry2013

Negative regulation of the acetyltransferase TIP60-p53 interplay by UHRF1 (ubiquitin-like with PHD and RING finger domains 1).

Chao Dai, Dingding Shi, Wei Gu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. The role of acetylation and deacetylation in cancer metabolism.Clinical and translational medicine · 2025
    Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Auranofin Protects Intestine against Radiation Injury by Modulating p53/p21 Pathway and Radiosensitizes Human Colon Tumor.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Interaction of the epigenetic integrator UHRF1 with the MYST domain of TIP60 inside the cell.Journal of experimental & clinical cancer research : CR · 2017
    Article
  17. Article
  18. Review
  19. Article
  20. Signalling pathways in UHRF1-dependent regulation of tumor suppressor genes in cancer.Journal of experimental & clinical cancer research : CR · 2016
    Review
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

3 authors at 2 institutions in 1 country.

Chao DaiInstitute for Cancer Genetics, Columbia University, New York, New York 10032, USA.
Dingding Shi
Wei Gu
Cancer Genetics (United States) · USHerbert Irving Comprehensive Cancer Center

Funding

PW1--A mediator of cell survival by NFKB and cell death by p53P01CA080058 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI AARONSON, STUART A · 2000 to 2016
$20.2M
CELL, MOLECULAR AND DEVELOPMENTAL BIOLOGY OF CANCERT32CA009503 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI GAUTIER, JEAN · 1985 to 2016
$6.8M
Regulation of p53 acetylation and deacetylation in tumorigenesis.R01CA085533 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2000 to 2021
$5.2M
Role of p53-mediated unconventional functions in tumor suppressionR01CA172023 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2012 to 2016
$1.6M
NCI NIH HHS 2P01 CA080058NCI NIH HHS 5R01 CA085533NCI NIH HHS 5R01 CA172023NCI NIH HHS P01 CA080058NCI NIH HHS R01 CA085533NCI NIH HHS R01 CA172023NCI NIH HHS T32 CA009503NCI NIH HHS T32-CA09503
6 · The paper itself

Abstract

Numerous studies indicate the importance of acetylation in p53-mediated stress responses upon DNA damage. We and others previously showed that TIP60 (Tat-interacting protein of 60 kDa)-mediated acetylation of p53 at K120 is crucial for p53-dependent apoptotic responses. Nevertheless, it remains unclear how TIP60-mediated effects on p53 are dynamically regulated in vivo. Here, we report that UHRF1 (ubiquitin-like with PHD and RING finger domains 1) interacts with TIP60 both in vitro and in vivo and induces degradation-independent ubiquitination of TIP60. Moreover, UHRF1 expression markedly suppresses the ability of TIP60 to acetylate p53. In contrast, RNAi-mediated knockdown of UHRF1 increases the endogenous levels of p53 acetylation at K120 and p53-mediated apoptosis is significantly enhanced in UHRF1-depleted cells. To elucidate the mechanisms of this regulation, we found that the interaction between TIP60 and p53 is severely inhibited in the presence of UHRF1, suggesting that UHRF1 modulates TIP60-mediated functions in both K120 acetylation-dependent and -independent manners. Consistent with this notion, UHRF1 knockdown promotes activation of p21 and PUMA but not MDM2. These findings demonstrate that UHRF1 is a critical negative regulator of TIP60 and suggest that UHRF1-mediated effects on p53 may contribute, at least in part, to its role in tumorigenesis.

Indexed as

ApoptosisUbiquitinationAcetylationApoptosis Regulatory ProteinsCCAAT-Enhancer-Binding ProteinsCell LineCell Transformation, NeoplasticGene Knockdown TechniquesHistone AcetyltransferasesHumansLysine Acetyltransferase 5Proto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53Ubiquitin-Protein LigasesApoptosis Regulatory ProteinsBBC3 protein, humanCCAAT-Enhancer-Binding ProteinsHistone AcetyltransferasesKAT5 protein, humanLysine Acetyltransferase 5MDM2 protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2TP53 protein, humanTumor Suppressor Protein p53Ubiquitin-Protein LigasesUHRF1 protein, humanAcetylationApoptosisGrowth ArrestOncogenep53TIP60Tumor Suppressor GeneUbiquitinationUHRF1

Identifiers

PMID23677994
PMCPMC3707659
OpenAlexW2045059096

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.