Evidence map›Paper›PMID 32351703›Full record

ArticleCell discovery2020

P53 suppresses SENP3 phosphorylation to mediate G2 checkpoint.

Yang Wang, Jing Tian, Chao Huang, Jiao Ma, Gaolei Hu, Yalan Chen, Tianshi Wang, Rong Cai, Yong Zuo, Hongsheng Tan and 7 more

Open access · goldAbstract read
In one paragraph

Article in Cell discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. AMPK activation coupling SENP1-Sirt3 axis protects against acute kidney injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. SUMOylation-Mediated Response to Mitochondrial Stress.International journal of molecular sciences · 2020
    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

17 authors at 2 institutions in 2 countries.

Yang Wang1Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, 200025 Shanghai, China.
Jing Tian1Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, 200025 Shanghai, China.
Chao Huang4Thoracic Oncology Institute at Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.ORCID 0000-0002-4913-921X
Jiao Ma1Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, 200025 Shanghai, China.
Gaolei Hu1Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, 200025 Shanghai, China.
Yalan Chen1Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, 200025 Shanghai, China.
Tianshi Wang1Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, 200025 Shanghai, China.
Rong Cai1Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, 200025 Shanghai, China.
Yong Zuo1Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, 200025 Shanghai, China.
Hongsheng Tan5School of Pharmacy, Shanghai University of Traditional Chinese Medicine, 201203 Shanghai, China.
Qiuju Fan1Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, 200025 Shanghai, China.
Baijun Dong1Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, 200025 Shanghai, China.
Wei Xue1Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, 200025 Shanghai, China.
Jing Yi1Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, 200025 Shanghai, China.
Guoqiang Chen2Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 200025 Shanghai, China.
Jun Tu1Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, 200025 Shanghai, China.
Jinke Cheng1Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, 200025 Shanghai, China.
Shanghai Jiao Tong University · CNShanghai University of Traditional Chinese Medicine · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31600664National Natural Science Foundation of China (National Science Foundation of China) 81430069National Natural Science Foundation of China (National Science Foundation of China) 81721004National Natural Science Foundation of China (National Science Foundation of China) 91229202
6 · The paper itself

Abstract

In response to DNA damage, p53-mediated signaling is regulated by protein phosphorylation and ubiquitination to precisely control G2 checkpoint. Here we demonstrated that protein SUMOylation also engaged in regulation of p53-mediated G2 checkpoint. We found that G2 DNA damage suppressed SENP3 phosphorylation at G2/M phases in p53-dependent manner. We further found that the suppression of SENP3 phosphorylation was crucial for efficient DNA damage/p53-induced G2 checkpoint and G2 arrest. Mechanistically, we identified Cdh1, a subunit of APC/C complex, was a SUMOylated protein at G2/M phase. SENP3 could de-SUMOylate Cdh1. DNA damage/p53-induced suppression of SENP3 phosphorylation activated SENP3 de-SUMOylation of Cdh. De-SUMOylation promoted Cdh1 de-phosphorylation by phosphatase Cdc14B, and then activated APC/C

Indexed as

Cell divisionSumoylation

Identifiers

PMID32351703
PMCPMC7171148
OpenAlexW3016633161

What OpenQuestion holds

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Registered trials

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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.