Evidence map›Paper›PMID 31691271›Full record

ArticleImmunology2020

Small-molecule inhibitors of ubiquitin-specific protease 7 enhance type-I interferon antiviral efficacy by destabilizing SOCS1.

Yukang Yuan, Ying Miao, Chenhua Zeng, Jin Liu, Xiangjie Chen, Liping Qian, Xiaofang Wang, Feng Qian, Zhengyuan Yu, Jun Wang and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Molecular Mechanisms of DUBs Regulation in Signaling and Disease.International journal of molecular sciences · 2021
    Review
  9. Article
  10. 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

14 authors at 1 institution in 2 countries.

Yukang YuanInstitutes of Biology and Medical Sciences, Jiangsu Key Laboratory of Infection and Immunity, Soochow University, Suzhou, China.
Ying MiaoInstitutes of Biology and Medical Sciences, Jiangsu Key Laboratory of Infection and Immunity, Soochow University, Suzhou, China.
Chenhua ZengInstitutes of Biology and Medical Sciences, Jiangsu Key Laboratory of Infection and Immunity, Soochow University, Suzhou, China.
Jin LiuInstitutes of Biology and Medical Sciences, Jiangsu Key Laboratory of Infection and Immunity, Soochow University, Suzhou, China.
Xiangjie ChenInstitutes of Biology and Medical Sciences, Jiangsu Key Laboratory of Infection and Immunity, Soochow University, Suzhou, China.
Liping QianInstitutes of Biology and Medical Sciences, Jiangsu Key Laboratory of Infection and Immunity, Soochow University, Suzhou, China.
Xiaofang WangInstitutes of Biology and Medical Sciences, Jiangsu Key Laboratory of Infection and Immunity, Soochow University, Suzhou, China.
Feng QianThe Affiliated Infectious Diseases Hospital of Soochow University, Suzhou, China.
Zhengyuan YuDepartment of Oncology, the First Affiliated Hospital of Soochow University, Suzhou, China.
Jun WangDepartment of Intensive Care Medicine, the First Affiliated Hospital of Soochow University, Suzhou, China.
Guanghui QianInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Qian FuSoochow University Library, Suzhou, China.
Haitao LvInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Hui ZhengInstitutes of Biology and Medical Sciences, Jiangsu Key Laboratory of Infection and Immunity, Soochow University, Suzhou, China.ORCID 0000-0002-4325-4946
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type-I interferons (IFN-I) are used as common antiviral drugs for a range of viral diseases in clinic. However, the antiviral efficacy of IFN-I is largely restricted by negative regulators of IFN-I signaling in cells. Therefore, identification of intracellular inhibitors of IFN-I signaling is important for developing novel targets to improve IFN-I antiviral therapy. In this study, we report that the deubiquitinase ubiquitin-specific protease 7 (USP7) negatively regulates IFN-I-mediated antiviral activity. USP7 physically interacts with suppressor of cytokine signaling 1 (SOCS1) and enhances SOCS1 protein stability by deubiquitination effects, which in turn restricts IFN-I-induced activation of Janus kinase-signal transducer and activator of transcription 1 signaling. Interestingly, viral infection up-regulates USP7 and therefore facilitates viral immune evasion. Importantly, the USP7 small-molecule inhibitors P5091 and P22077 inhibit SOCS1 expression and enhance IFN-I antiviral efficacy. Our findings identify a novel regulator of IFN-I antiviral activity and reveal that USP7 inhibitors could be potential enhancement agents for improving IFN-I antiviral therapy.

Indexed as

A549 CellsAntiviral AgentsEnzyme InhibitorsHEK293 CellsHeLa CellsHost-Pathogen InteractionsHumansInfluenza A Virus, H1N1 SubtypeInterferon-alphaJanus KinasesProtein BindingProtein StabilityProteolysisSignal TransductionSuppressor of Cytokine Signaling 1 ProteinThiophenes1-(5-((2,4-difluorophenyl)thio)-4-nitrothiophen-2-yl)ethanoneAntiviral AgentsEnzyme InhibitorsInterferon-alphaJanus KinasesP5091SOCS1 protein, humanSuppressor of Cytokine Signaling 1 ProteinThiophenesUbiquitin-Specific Peptidase 7USP7 protein, humanantiviral activityinterferonsmall-molecule inhibitorsuppressor of cytokine signaling 1ubiquitin-specific protease 7

Identifiers

PMID31691271
PMCPMC7011631
OpenAlexW2983540832

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.