Evidence map›Paper›PMID 31899788›Full record

ArticlePLoS pathogens2020

USP12 translocation maintains interferon antiviral efficacy by inhibiting CBP acetyltransferase activity.

Jin Liu, Lincong Jin, Xiangjie Chen, Yukang Yuan, Yibo Zuo, Ying Miao, Qian Feng, Hongguang Zhang, Fan Huang, Tingting Guo and 5 more

Abstract read
In one paragraph

Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. USP12 promotes CD4Cell death and differentiation · 2021
    Article
  13. Article
  14. Review
  15. 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

15 authors.

Jin LiuInternational Institute of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China.
Lincong JinInternational Institute of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China.
Xiangjie ChenInternational Institute of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China.
Yukang YuanInternational Institute of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China.
Yibo ZuoInternational Institute of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China.
Ying MiaoInternational Institute of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China.
Qian FengInternational Institute of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China.
Hongguang ZhangInternational Institute of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China.
Fan HuangInternational Institute of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China.
Tingting GuoInternational Institute of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China.
Liting ZhangInternational Institute of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China.
Li ZhuThe Affiliated Infectious Diseases Hospital of Soochow University, Suzhou, China.
Feng QianThe Affiliated Infectious Diseases Hospital of Soochow University, Suzhou, China.
Chuanwu ZhuThe Affiliated Infectious Diseases Hospital of Soochow University, Suzhou, China.ORCID 0000-0002-9113-2046
Hui ZhengInternational Institute of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China.ORCID 0000-0002-4325-4946

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CREB-binding protein (CBP) participates in numerous transcription events. However, cell-intrinsic inhibitors of CBP are poorly defined. Here, we found that cellular USP12 interacts with the HAT domain of CBP and inhibits CBP's acetyltransferase activity. Interestingly, USP12 positively regulates interferon (IFN) antiviral signaling independently of its deubiquitinase activity. Furthermore, we found that in IFN signaling USP12 translocates from the cytoplasm to the nucleus. The decrease in cytoplasmic USP12 facilitates CBP-induced acetylation and activation of IFN signaling proteins in the cytoplasm. Moreover, USP12 accumulation in the nucleus blocks CBP-induced acetylation of phosphorylated STAT1 (p-STAT1) and therefore inhibits the dephosphorylation effects of TCPTP on p-STAT1, which finally maintains nuclear p-STAT1 levels and IFN antiviral efficacy. USP12 nuclear translocation extends our understanding of the regulation of the strength of IFN antiviral signaling. Our study uncovers a cell-intrinsic regulation of CBP acetyltransferase activity and may provide potential strategies for IFN-based antiviral therapy.

Indexed as

AcetylationAnimalsAntiviral AgentsCREB-Binding ProteinCytoplasmEnzyme InhibitorsHCT116 CellsHEK293 CellsHeLa CellsHumansInterferonsMiceMice, Inbred C57BLProtein DomainsRAW 264.7 CellsSignal TransductionAntiviral AgentsCREB-Binding ProteinCrebbp protein, mouseEnzyme InhibitorsInterferonsStat1 protein, mouseSTAT1 Transcription FactorUbiquitin ThiolesteraseUsp12 protein, mouse

Identifiers

PMID31899788
PMCPMC6961928

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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.