Evidence map›Paper›PMID 24289924›Full record

ArticleMolecular cell2014

Phosphorylation of p53 by TAF1 inactivates p53-dependent transcription in the DNA damage response.

Yong Wu, Joy C Lin, Landon G Piluso, Joseph M Dhahbi, Selene Bobadilla, Stephen R Spindler, Xuan Liu

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.1field-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

40 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
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  11. Article
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  13. Article
  14. Deciphering the PTM codes of the tumor suppressor p53.Journal of molecular cell biology · 2022
    Review
  15. Article
  16. Tumor suppressor p53: Biology, signaling pathways, and therapeutic targeting.Biochimica et biophysica acta. Reviews on cancer · 2021
    Review
  17. Article
  18. Article
  19. Article
  20. A phosphorylation-dependent switch in the disordered p53 transactivation domain regulates DNA binding.Proceedings of the National Academy of Sciences of the United States of America · 2021
    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 1 institution in 1 country.

Yong WuDepartment of Biochemistry, University of California, Riverside, Riverside, CA 92521, USA.
Joy C LinDepartment of Biochemistry, University of California, Riverside, Riverside, CA 92521, USA.
Landon G PilusoDepartment of Biochemistry, University of California, Riverside, Riverside, CA 92521, USA.
Joseph M DhahbiDepartment of Biochemistry, University of California, Riverside, Riverside, CA 92521, USA.
Selene BobadillaDepartment of Biochemistry, University of California, Riverside, Riverside, CA 92521, USA.
Stephen R SpindlerDepartment of Biochemistry, University of California, Riverside, Riverside, CA 92521, USA.
Xuan LiuDepartment of Biochemistry, University of California, Riverside, Riverside, CA 92521, USA. Electronic address: xuan.liu@ucr.edu.
University of California, Riverside · US

Funding

Regulation of p53 by TAFII250R01CA075180 · NCI · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI LIU, XUAN · 2002 to 2020
$4.7M
Genome wide analysis of p53 inhibition by high glucoseF31CA177219 · NCI · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI BOBADILLA, SELENE · 2013 to 2017
$187k
Regulation of p53 by BRCA1 in Breast CancerF32CA144214 · NCI · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI LIN, JOY CHIEH-YU · 2010 to 2013
$164k
NCI NIH HHS F31 CA177219NCI NIH HHS F31CA177219NCI NIH HHS F32 CA144214NCI NIH HHS F32CA144214NCI NIH HHS R01 CA075180NCI NIH HHS R01CA075180
6 · The paper itself

Abstract

While p53 activation has long been studied, the mechanisms by which its targets genes are restored to their preactivation state are less clear. We report here that TAF1 phosphorylates p53 at Thr55, leading to dissociation of p53 from the p21 promoter and inactivation of transcription late in the DNA damage response. We further show that cellular ATP level might act as a molecular switch for Thr55 phosphorylation on the p21 promoter, indicating that TAF1 is a cellular ATP sensor. Upon DNA damage, cells undergo PARP-1-dependent ATP depletion, which is correlated with reduced TAF1 kinase activity and Thr55 phosphorylation, resulting in p21 activation. As cellular ATP levels recover, TAF1 is able to phosphorylate p53 on Thr55, which leads to dissociation of p53 from the p21 promoter. ChIP-sequencing analysis reveals p53 dissociates from promoters genome wide as cells recover from DNA damage, suggesting the general nature of this mechanism.

Indexed as

DNA DamagePromoter Regions, GeneticTranscription, GeneticAdenosine TriphosphateCell LineCyclin-Dependent Kinase Inhibitor p21Genome-Wide Association StudyHistone AcetyltransferasesHumansPhosphorylationTATA-Binding Protein Associated FactorsTranscription Factor TFIIDTumor Suppressor Protein p53Adenosine TriphosphateCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Histone AcetyltransferasesTATA-binding protein associated factor 250 kDaTATA-Binding Protein Associated FactorsTP53 protein, humanTranscription Factor TFIIDTumor Suppressor Protein p53

Identifiers

PMID24289924
PMCPMC3919457
OpenAlexW2073631639

What OpenQuestion holds

Textmetadata
LicenceTDM
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.