Evidence map›Paper›PMID 31241013›Full record

ArticleAutophagy2020

The ubiquitin-specific protease USP8 directly deubiquitinates SQSTM1/p62 to suppress its autophagic activity.

Hong Peng, Fang Yang, Qianwen Hu, Jian Sun, Cheng Peng, Yao Zhao, Chuanxin Huang

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

65 citing papers in PubMed, 136 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. The value of targeting CXCR4 withEuropean journal of nuclear medicine and molecular imaging · 2026
    Article
  7. Review
  8. Article
  9. The Roles of SQSTM1/p62 in Selective Autophagy and Oncogenic Signaling.International journal of molecular sciences · 2026
    Review
  10. Article
  11. Article
  12. Review
  13. Inducing ferroptosis to improve cancer therapy: a promising tool for enhancing immunotherapy.Journal of experimental & clinical cancer research : CR · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

5 more citing papers are in PubMed but not listed here.

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 4 institutions in 1 country.

Hong PengShanghai Institute of Immunology & Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Faculty of Basic Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Fang YangShanghai Institute of Immunology & Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Faculty of Basic Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Qianwen HuShanghai Institute of Immunology & Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Faculty of Basic Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jian SunDepartment of Breast Surgery, Obstetrics and Gynecology Hospital, Fudan University, Shanghai, China.
Cheng PengShanghai Institute of Immunology & Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Faculty of Basic Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yao ZhaoDepartment of Neurosurgery, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Chuanxin HuangShanghai Institute of Immunology & Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Faculty of Basic Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0003-2667-9587
Shanghai Jiao Tong University · CNFudan University · CNObstetrics and Gynecology Hospital of Fudan University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SQSTM1/p62 (sequestosome 1) is a critical macroautophagy/autophagy receptor that promotes the formation and degradation of ubiquitinated aggregates. SQSTM1 can be modified by ubiquitination, and this modification modulates its autophagic activity. However, the molecular mechanisms underpinning its reversible deubiquitination have never been described. Here we report that USP8 (ubiquitin specific peptidase 8) directly interacted with and deubiquitinated SQSTM1. USP8 preferentially removed the lysine 11 (K11)-linked ubiquitin chains from SQSTM1. Moreover, USP8 deubiquitinated SQSTM1 principally at K420 within its ubiquitin-association (UBA) domain. Finally, USP8 inhibited SQSTM1 degradation and autophagic influx in cells with wild-type SQSTM1, but not its mutant with substitution of K420 with an arginine. Taken together, USP8 acts as a negative regulator of autophagy by deubiquitinating SQSTM1 at K420.

Indexed as

AutophagyEndopeptidasesEndosomal Sorting Complexes Required for TransportHumansKelch-Like ECH-Associated Protein 1Protein DomainsSequestosome-1 ProteinUbiquitinUbiquitinationUbiquitin-Specific ProteasesUbiquitin ThiolesteraseEndopeptidasesEndosomal Sorting Complexes Required for TransportKelch-Like ECH-Associated Protein 1Sequestosome-1 ProteinSQSTM1 protein, humanUbiquitinUbiquitin-Specific ProteasesUbiquitin ThiolesteraseUSP8 protein, humanAutophagydegradationSQSTM1/p62ubiquitinationUSP8

Identifiers

PMID31241013
PMCPMC7138243
OpenAlexW2954137892

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.