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Article

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

1
Division of Clinical Cancer Research, Research Institute, National Cancer Center, Goyang 10408, Korea
2
Department of Pediatrics, University of Texas Medical Branch, Galveston, TX 77555, USA
3
Department of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea
4
Department of Life Science and Multidisciplinary Genome Institute, Hallym University, Chuncheon 24252, Korea
5
Personalized Genomic Medicine Research Center, KRIBB, Daejeon 34141, Korea
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Department of Functional Genomics, University of Science and Technology, Daejeon 34113, Korea
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Division of Thoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, TX 77030, USA
8
Department of Systems Biology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
*
Author to whom correspondence should be addressed.
Academic Editor: Li Lin
Int. J. Mol. Sci. 2021, 22(4), 2003; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22042003
Received: 26 January 2021 / Revised: 9 February 2021 / Accepted: 9 February 2021 / Published: 18 February 2021
(This article belongs to the Special Issue Non-coding RNAs in Pathogen-Host Interaction)
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. View Full-Text
Keywords: nc886; pathogen; interferon; Protein Kinase R; Interferon Regulatory Factor 3 nc886; pathogen; interferon; Protein Kinase R; Interferon Regulatory Factor 3
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MDPI and ACS Style

Lee, Y.-S.; Bao, X.; Lee, H.-H.; Jang, J.J.; Saruuldalai, E.; Park, G.; Im, W.R.; Park, J.-L.; Kim, S.-Y.; Shin, S.; Jeon, S.H.; Kang, S.; Lee, H.-S.; Lee, J.-S.; Zhang, K.; Park, E.J.; Kim, I.-H.; Lee, Y.S. Nc886, a Novel Suppressor of the Type I Interferon Response Upon Pathogen Intrusion. Int. J. Mol. Sci. 2021, 22, 2003. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22042003

AMA Style

Lee Y-S, Bao X, Lee H-H, Jang JJ, Saruuldalai E, Park G, Im WR, Park J-L, Kim S-Y, Shin S, Jeon SH, Kang S, Lee H-S, Lee J-S, Zhang K, Park EJ, Kim I-H, Lee YS. Nc886, a Novel Suppressor of the Type I Interferon Response Upon Pathogen Intrusion. International Journal of Molecular Sciences. 2021; 22(4):2003. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22042003

Chicago/Turabian Style

Lee, Yeon-Su, Xiaoyong Bao, Hwi-Ho Lee, Jiyoung J. Jang, Enkhjin Saruuldalai, Gaeul Park, Wonkyun R. Im, Jong-Lyul Park, Seon-Young Kim, Sooyong Shin, Sung H. Jeon, Sangmin Kang, Hyun-Sung Lee, Ju-Seog Lee, Ke Zhang, Eun J. Park, In-Hoo Kim, and Yong S. Lee 2021. "Nc886, a Novel Suppressor of the Type I Interferon Response Upon Pathogen Intrusion" International Journal of Molecular Sciences 22, no. 4: 2003. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22042003

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