Evidence map›Paper›PMID 33670458›Full record

ArticleInternational journal of molecular sciences2021

Nc886, a Novel Suppressor of the Type I Interferon Response Upon Pathogen Intrusion.

Yeon-Su Lee, Xiaoyong Bao, Hwi-Ho Lee, Jiyoung Joan Jang, Enkhjin Saruuldalai, Gaeul Park, Wonkyun Ronny Im, Jong-Lyul Park, Seon-Young Kim, Sooyong Shin and 8 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Non-coding 886 (Epigenetics · 2024
    Review
  5. Article
  6. Review
  7. Article
  8. Human Vault RNAs: Exploring Their Potential Role in Cellular Metabolism.International journal of molecular sciences · 2024
    Review
  9. Review
  10. Review
  11. Review
  12. Hypermethylation ofMolecular therapy. Nucleic acids · 2022
    Article
  13. Review
  14. Are We Studying Non-Coding RNAs Correctly? Lessons from nc886.International journal of molecular sciences · 2022
    Review
  15. Article
  16. Article
  17. Editorial of Special Issue "Non-Coding RNAs in Pathogen-Host Interaction".International journal of molecular sciences · 2021
    Article
  18. 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

18 authors at 5 institutions in 2 countries.

Yeon-Su LeeDivision of Clinical Cancer Research, Research Institute, National Cancer Center, Goyang 10408, Korea.
Xiaoyong BaoDepartment of Pediatrics, University of Texas Medical Branch, Galveston, TX 77555, USA.ORCID 0000-0002-6884-2584
Hwi-Ho LeeDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea.
Jiyoung Joan JangDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea.
Enkhjin SaruuldalaiDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea.
Gaeul ParkDivision of Clinical Cancer Research, Research Institute, National Cancer Center, Goyang 10408, Korea.
Wonkyun Ronny ImDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea.
Jong-Lyul ParkPersonalized Genomic Medicine Research Center, KRIBB, Daejeon 34141, Korea.
Seon-Young KimPersonalized Genomic Medicine Research Center, KRIBB, Daejeon 34141, Korea.
Sooyong ShinDepartment of Life Science and Multidisciplinary Genome Institute, Hallym University, Chuncheon 24252, Korea.
Sung Ho JeonDepartment of Life Science and Multidisciplinary Genome Institute, Hallym University, Chuncheon 24252, Korea.ORCID 0000-0001-5982-140X
Sangmin KangDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea.
Hyun-Sung LeeDivision of Thoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, TX 77030, USA.ORCID 0000-0001-8259-046X
Ju-Seog LeeDepartment of Systems Biology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.ORCID 0000-0002-5666-9753
Ke ZhangDepartment of Pediatrics, University of Texas Medical Branch, Galveston, TX 77555, USA.
Eun Jung ParkDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea.
In-Hoo KimDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea.
Yong Sun LeeDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea.ORCID 0000-0001-9689-3410
National Cancer Center · KRHallym University · KRBaylor College of Medicine · USThe University of Texas MD Anderson Cancer Center · USKorea Research Institute of Bioscience and Biotechnology · KR

Funding

National Research Foundation of Korea NRF-2017M3C9A6044517National Research Foundation of Korea NRF-2019R1A2C2088108
6 · The paper itself

Abstract

Interferons (IFNs) are a crucial component in the innate immune response. Especially the IFN-β signaling operates in most cell types and plays a key role in the first line of defense upon pathogen intrusion. The induction of IFN-β should be tightly controlled, because its hyperactivation can lead to tissue damage or autoimmune diseases. Activation of the IFN-β promoter needs Interferon Regulatory Factor 3 (IRF3), together with Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB) and Activator Protein 1 (AP-1). Here we report that a human noncoding RNA, nc886, is a novel suppressor for the IFN-β signaling and inflammation. Upon treatment with several pathogen-associated molecular patterns and viruses, nc886 suppresses the activation of IRF3 and also inhibits NF-κB and AP-1 via inhibiting Protein Kinase R (PKR). These events lead to decreased expression of IFN-β and resultantly IFN-stimulated genes. nc886's role might be to restrict the IFN-β signaling from hyperactivation. Since nc886 expression is regulated by epigenetic and environmental factors, nc886 might explain why innate immune responses to pathogens are variable depending on biological settings.

Indexed as

AnimalsCell Line, TumoreIF-2 KinaseGene Expression RegulationHCT116 CellsHEK293 CellsHost-Pathogen InteractionsHumansImmunity, InnateInterferon Regulatory Factor-3Interferon Type IMiceNF-kappa BPromoter Regions, GeneticRAW 264.7 CellsRNA, UntranslatedeIF-2 KinaseInterferon Regulatory Factor-3Interferon Type INF-kappa BRNA, UntranslatedTranscription Factor AP-1interferonInterferon Regulatory Factor 3nc886pathogenProtein Kinase R

Identifiers

PMID33670458
PMCPMC7922379
OpenAlexW3132112317

What OpenQuestion holds

Textmetadata
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.