Evidence map›Paper›PMID 27517492›Full record

ArticleOncotarget2017

USP19 deubiquitinates HDAC1/2 to regulate DNA damage repair and control chromosomal stability.

Min Wu, Hai-Qing Tu, Yan Chang, Bo Tan, Guang Wang, Jie Zhou, Li Wang, Rui Mu, Wei-Na Zhang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Deubiquitylating Enzymes in Cancer and Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Review
  5. Article
  6. Article
  7. Review
  8. HDAC2 as a target for developing anti-cancer drugs.Computational and structural biotechnology journal · 2023
    Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Cancers · 2021
    Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

9 authors at 2 institutions in 1 country.

Min WuState Key Laboratory of Proteomics, National Center of Biomedical Analysis, Institute of BasicMedical Sciences, Beijing 100850, China.
Hai-Qing TuState Key Laboratory of Proteomics, National Center of Biomedical Analysis, Institute of BasicMedical Sciences, Beijing 100850, China.
Yan ChangState Key Laboratory of Proteomics, National Center of Biomedical Analysis, Institute of BasicMedical Sciences, Beijing 100850, China.
Bo TanState Key Laboratory of Proteomics, National Center of Biomedical Analysis, Institute of BasicMedical Sciences, Beijing 100850, China.
Guang WangState Key Laboratory of Proteomics, National Center of Biomedical Analysis, Institute of BasicMedical Sciences, Beijing 100850, China.
Jie ZhouState Key Laboratory of Proteomics, National Center of Biomedical Analysis, Institute of BasicMedical Sciences, Beijing 100850, China.
Li WangState Key Laboratory of Proteomics, National Center of Biomedical Analysis, Institute of BasicMedical Sciences, Beijing 100850, China.
Rui MuDepartment of Radiation Oncology, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.
Wei-Na ZhangState Key Laboratory of Proteomics, National Center of Biomedical Analysis, Institute of BasicMedical Sciences, Beijing 100850, China.
National Center of Biomedical Analysis · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive accumulation of DNA damage will generate chromosome stress, leading to various chromosome abnormalities such as chromatin bridge and result in genomic instability. Orchestra procession and regulation of DNA damage repair are vital for keeping genome stability. Despite of the key role of HDAC1/2 in double strand break (DSB) repair, the regulation for their mode of action is less well understood. In this study, we found that deubiquitination enzymes USP19 physically interacts with HDAC1/2 and specifically regulate their K63-linked ubiquitination, which might be crucial for regulation of HDAC1/2 activity in DNA damage repair. Notably, we found that USP19 trans-locate into nucleus upon IR irradiation and is indispensable for normally DNA damage response. In addition, we showed that USP19 play critical role in preventing anaphase bridge formation through regulating DNA damage repair process. Furthermore, the expression level of USP19 is commonly lower or deleted in several types of tumor. These results indicated that USP19 is a key factor in modulating DNA damage repair by targeting HDAC1/2 K63-linked ubiquitination, cells with deletion or decreased expression of USP19 might cause genome instability and even contribute to tumorigenesis.

Indexed as

UbiquitinationCarcinogenesisCell Line, TumorDeubiquitinating EnzymesDNA DamageDNA RepairEndopeptidasesGenomic InstabilityHCT116 CellsHEK293 CellsHeLa CellsHistone Deacetylase 1Histone Deacetylase 2HumansProtein Processing, Post-TranslationalDeubiquitinating EnzymesEndopeptidasesHDAC1 protein, humanHDAC2 protein, humanHistone Deacetylase 1Histone Deacetylase 2USP19 protein, humanDNA repairgenome stabilityHDAC1/2USP19

Identifiers

PMID27517492
PMCPMC5356792
OpenAlexW2517531299

What OpenQuestion holds

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LicenceCC BY
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.