ArticleNature communications2018
Downregulated NDR1 protein kinase inhibits innate immune response by initiating an miR146a-STAT1 feedback loop.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Antiviral drug discovery and development: challenges and future directions.Signal transduction and targeted therapy · 2026Review
- SCRN1 confers hepatocellular carcinoma resistance to ferroptosis by stabilizing GPX4 via STK38-mediated phosphorylation.Nature cancer · 2025Article
- NDR2 Kinase Regulates Microglial Metabolic Adaptation and Inflammatory Response: Critical Role in Glucose-Dependent Functional Plasticity.International journal of molecular sciences · 2025Article
- Mechanisms underlying TRPV4-mediated regulation of miR-146a expression.Frontiers in immunology · 2024Article
- The Association between Four Common Polymorphisms in microRNA and Risk of Hepatocellular Carcinoma: An Updated Meta-Analysis.Iranian journal of public health · 2023Review
- Review
- MicroRNAs in Macrophages: Regulators of Activation and Function.Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- Review
- NDR1 activates CD47 transcription by increasing protein stability and nuclear location of ASCL1 to enhance cancer stem cell properties and evasion of phagocytosis in small cell lung cancer.Medical oncology (Northwood, London, England) · 2022Article
- Prognostic and Immunological Role ofInternational journal of molecular sciences · 2022Article
- Review
- African swine fever virus MGF360-11L negatively regulates cGAS-STING-mediated inhibition of type I interferon production.Veterinary research · 2022Article
- Molecular Mechanism of Biofilm Locator Protein Kinase Dbf2p-related kinase 1 in Regulating Innate Immune Response to Interleukin 17-induced Viral Pneumonia.Bioengineered · 2021Article
- The STK38-XPO1 axis, a new actor in physiology and cancer.Cellular and molecular life sciences : CMLS · 2021Review
- IgY - turning the page toward passive immunization in COVID-19 infection (Review).Experimental and therapeutic medicine · 2020Review
- Review
- Xuebijing Injection Alleviates Pam3CSK4-Induced Inflammatory Response and Protects Mice From Sepsis Caused by Methicillin-ResistantFrontiers in pharmacology · 2020Article
- The Emerging Roles of NDR1/2 in Infection and Inflammation.Frontiers in immunology · 2020Review
- NDR2 promotes the antiviral immune response via facilitating TRIM25-mediated RIG-I activation in macrophages.Science advances · 2019Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interferon (IFN)-stimulated genes (ISGs) play crucial roles in the antiviral immune response; however, IFNs also induce negative regulators that attenuate the antiviral response. Here, we show that both viral and bacterial invasion downregulate Nuclear Dbf2-related kinase 1 (NDR1) expression via the type I IFN signaling pathway. NDR1 promotes the virus-induced production of type I IFN, proinflammatory cytokines and ISGs in a kinase-independent manner. NDR1 deficiency also renders mice more susceptible to viral and bacterial infections. Mechanistically, NDR1 enhances STAT1 translation by directly binding to the intergenic region of miR146a, thereby inhibiting miR146a expression and liberating STAT1 from miR146a-mediated translational inhibition. Furthermore, STAT1 binds to the miR146a promoter, thus decreasing its expression. Together, our results suggest that NDR1 promotion of STAT1 translation is an important event for IFN-dependent antiviral immune response, and suggest that NDR1 has an important role in controlling viral infections.
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Registered trials
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.