Evidence map›Paper›PMID 35394840›Full record

ArticleScience advances2022

LATS1 is a central signal transmitter for achieving full type-I interferon activity.

Yibo Zuo, Jiuyi He, Siying Liu, Ying Xu, Jin Liu, Caixia Qiao, Lichao Zang, Wenhuan Sun, Yukang Yuan, Hongguang Zhang and 13 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Role ofCancers · 2024
    Review
  8. Transcriptional control of interferon-stimulated genes.The Journal of biological chemistry · 2024
    Review
  9. The NDR family of kinases: essential regulators of aging.Frontiers in molecular neuroscience · 2024
    Review
  10. Article
  11. Article
  12. ADP-Ribosylation in Antiviral Innate Immune Response.Pathogens (Basel, Switzerland) · 2023
    Review
  13. 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

23 authors at 3 institutions in 2 countries.

Yibo ZuoInternational Institute of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China.ORCID 0000-0003-1908-6054
Jiuyi HeInternational Institute of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China.
Siying LiuCAMS Key Laboratory of Synthetic Biology Regulatory Elements, Institute of Systems Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Ying XuDepartment of Intensive Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.
Jin LiuThe Affiliated Infectious Diseases Hospital of Soochow University, Suzhou, Jiangsu, China.
Caixia QiaoInternational Institute of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China.
Lichao ZangDepartment of Laboratory Medicine, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China.
Wenhuan SunInternational 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.
Hongguang ZhangInternational 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.
Lincong JinInternational 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.
Fan HuangInternational Institute of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China.
Tengfei RenInternational Institute of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China.
Jun WangDepartment of Intensive Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.ORCID 0000-0001-8708-3096
Feng QianThe Affiliated Infectious Diseases Hospital of Soochow University, Suzhou, Jiangsu, China.
Chuanwu ZhuThe Affiliated Infectious Diseases Hospital of Soochow University, Suzhou, Jiangsu, China.ORCID 0000-0002-9113-2046
Wei ZhangDepartment of Molecular and Cellular Biology, College of Biological Science, University of Guelph, Guelph, Ontario, N1G2W1, Canada.
Yaobo LiuJiangsu Key Laboratory of Neuropsychiatric Diseases and Institute of Neuroscience, Soochow University, Suzhou, Jiangsu, China.ORCID 0000-0002-7663-5649
Guoqiang XuCollege of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu 215123, China.ORCID 0000-0002-4753-4769
Feng MaCAMS Key Laboratory of Synthetic Biology Regulatory Elements, Institute of Systems Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0002-2975-0118
Hui ZhengInternational Institute of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China.ORCID 0000-0002-4325-4946
Soochow University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNUniversity of Guelph · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interferons (IFNs) have broad-spectrum antiviral activity to resist virus epidemic. However, IFN antiviral efficacy needs to be greatly improved. Here, we reveal that LATS1 is a vital signal transmitter governing full type-I IFN (IFN-I) signaling activity. LATS1 constitutively binds with the IFN-I receptor IFNAR2 and is rapidly tyro-phosphorylated by Tyk2 upon IFN-I engagement. Tyro-phosphorylation of LATS1 promotes LATS1 activation and YAP degradation, thereby promoting IFN-mediated antiproliferation activity. Moreover, activated LATS1 translocates into the nucleus and induces CDK8-Ser62 phosphorylation, which in turn phosphorylates STAT1 at Ser

Identifiers

PMID35394840
PMCPMC8993116
OpenAlexW4223476013

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.