Evidence map›Paper›PMID 28673515›Full record

ArticleBiochimica et biophysica acta. Molecular basis of disease2017

High glucose-induced p53 phosphorylation contributes to impairment of endothelial antioxidant system.

Yong Wu, Sangkyu Lee, Selene Bobadilla, Sheng Zhong Duan, Xuan Liu

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta. Molecular basis of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

26 citing papers in PubMed, 33 citations in OpenAlex.

  1. CD4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  8. Transcriptomic signature related to poor welfare of sport horses.Comprehensive psychoneuroendocrinology · 2023
    Article
  9. Article
  10. Review
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  15. Article
  16. Article
  17. Effects ofFood science & nutrition · 2020
    Article
  18. Review
  19. Article
  20. 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

5 authors at 2 institutions in 2 countries.

Yong WuDepartment of Biochemistry, University of California, Riverside, CA 92521, United States.
Sangkyu LeeDepartment of Biochemistry, University of California, Riverside, CA 92521, United States.
Selene BobadillaDepartment of Biochemistry, University of California, Riverside, CA 92521, United States.
Sheng Zhong DuanKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai, People's Republic of China; Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, People's Republic of China.
Xuan LiuDepartment of Biochemistry, University of California, Riverside, CA 92521, United States. Electronic address: xuan.liu@ucr.edu.
University of California, Riverside · USChinese Academy of Sciences · CN

Funding

Regulation of p53 by TAFII250R01CA075180 · NCI · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI LIU, XUAN · 2002 to 2020
$4.7M
Mechanisms behind hyperglycemia-associated breast cancer risk and progressionSC1CA200517 · NCI · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI WU, YONG · 2015 to 2018
$1.4M
REGULATION OF P53 DEPENDENT TRANSCRIPTION BY C-AB1R29CA075180 · NCI · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI LIU, XUAN · 1997 to 2001
$203k
Genome wide analysis of p53 inhibition by high glucoseF31CA177219 · NCI · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI BOBADILLA, SELENE · 2013 to 2017
$187k
NCI NIH HHS F31 CA177219NCI NIH HHS R01 CA075180NCI NIH HHS R29 CA075180NCI NIH HHS SC1 CA200517
6 · The paper itself

Abstract

High levels of glucose (HG) induce reactive oxygen species-mediated oxidative stress in endothelial cells (ECs), which leads to endothelial dysfunction and tissue damage. However, the molecular mechanisms involved in HG-induced endothelial oxidative stress and damage remain elusive. Here we show that cellular ATP level-modulated p53 Thr55 phosphorylation plays a critical role in the process. Upon HG exposure, the elevated ATP levels induced the kinase activity of TAF1 (TBP-associated factor 1), which leads to p53 Thr55 phosphorylation. The phosphorylation dissociates p53 from the glutathione peroxidase 1 (GPX1) promoter and results in reduction of GPX1 expression. Inhibition of TAF1-mediated p53 Thr55 phosphorylation abolished those events, supporting the role of TAF1 in sensing cellular ATP elevation and in regulating GPX1 expression under the HG condition. Importantly, treating cells with HG increased intracellular H

Indexed as

Adenosine TriphosphateAntioxidantsCardiovascular DiseasesDiabetes ComplicationsGlucoseGlutathione PeroxidaseGlutathione Peroxidase GPX1Histone AcetyltransferasesHumansHuman Umbilical Vein Endothelial CellsHydrogen PeroxideNitric OxidePhosphorylationTATA-Binding Protein Associated FactorsTranscription Factor TFIIDTumor Suppressor Protein p53Adenosine TriphosphateAntioxidantsGlucoseGlutathione PeroxidaseGlutathione Peroxidase GPX1GPX1 protein, humanHistone AcetyltransferasesHydrogen PeroxideNitric OxideTATA-binding protein associated factor 250 kDaTATA-Binding Protein Associated FactorsTP53 protein, humanTranscription Factor TFIIDTumor Suppressor Protein p53Cellular ATPGPX1High glucosep53TAF1Thr55 phosphorylation

Identifiers

PMID28673515
PMCPMC5939960
OpenAlexW2730503059

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.