Evidence map›Paper›PMID 41913215›Full record

ArticleCell communication and signaling : CCS2026

TBK1-NQO1 negative feedback loop regulates antiviral innate immunity.

Hyuncheol Lee, Asela Weerawardhana, Kiramage Chathuranga, W A Gayan Chathuranga, Tae-Hwan Kim, Duk-Jae Jang, Aleysha Chen, David Schaffer, Jae U Jung, Chul-Ho Lee and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

11 authors.

Hyuncheol Lee *Laboratory of Microbiology, College of Veterinary Medicine, Chungnam National University, Daejeon, Republic of Korea.
Asela Weerawardhana *Laboratory of Microbiology, College of Veterinary Medicine, Chungnam National University, Daejeon, Republic of Korea.ORCID http://orcid.org/0000-0002-7412-5450
Kiramage ChathurangaLaboratory of Microbiology, College of Veterinary Medicine, Chungnam National University, Daejeon, Republic of Korea.
W A Gayan ChathurangaLaboratory of Microbiology, College of Veterinary Medicine, Chungnam National University, Daejeon, Republic of Korea.
Tae-Hwan KimLaboratory of Microbiology, College of Veterinary Medicine, Chungnam National University, Daejeon, Republic of Korea.
Duk-Jae JangLaboratory of Microbiology, College of Veterinary Medicine, Chungnam National University, Daejeon, Republic of Korea.
Aleysha ChenDepartment of Bioengineering, University of California, Berkeley, Berkeley, CA, 94720, USA.
David SchafferCalifornia Institute for Quantitative Biosciences, University of California, Berkeley, CA, 94720, USA.
Jae U JungDepartment of Cancer Biology, Infection Biology Program, and Global Center for Pathogen Research and Human Health, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Chul-Ho LeeLaboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology, University of Science and Technology (UST), Daejeon, Republic of Korea.
Jong-Soo LeeLaboratory of Microbiology, College of Veterinary Medicine, Chungnam National University, Daejeon, Republic of Korea. jongsool@cnu.ac.kr.ORCID http://orcid.org/0000-0001-5119-0711

Funding

Institute for Basic Science IBS-R801-D9-A01National Research Foundation of Korea RS-2021-NR060136
6 · The paper itself

Abstract

TANK-binding kinase 1 (TBK1) is an essential kinase that phosphorylates transcriptional factors, which induce antiviral interferons and inflammatory cytokines against viral infection. Tight regulation of TBK1 is critical for innate immune responses and maintenance of homeostasis. Here, we report that NAD(P)H: quinone-oxidoreductase-1 (NQO1) forms a negative feedback loop with TBK1 to regulate innate antiviral immune responses. At the late time stages of virus infection, NQO1 specifically interacts with TBK1 and is phosphorylated at S82 of NQOI by TBK1. Interestingly, S82-phosphorylated NQO1 interferes with the self-association and phosphorylation of TBK1, resulting in reduced type I IFN signaling cascades. Depletion or reduced expression of NQO1 increases secretion of antiviral cytokines and resultes in less viral replication. In particular, NQO1−/− mice are more resistant to viral infection due to the enhanced secretion of antiviral cytokines. Taken together, these finding provide new insight into the molecular regulation of NQOI and TBK1 and suggest a critical role for NQOI in the homeostatic control of antiviral response and innate immune responses.

Indexed as

Feedback, PhysiologicalImmunity, InnateNAD(P)H Dehydrogenase (Quinone)Protein Serine-Threonine KinasesAnimalsHEK293 CellsHumansInterferon Type IMicePhosphorylationProtein BindingSignal TransductionInterferon Type INAD(P)H Dehydrogenase (Quinone)NQO1 protein, humanNqo1 protein, mouseProtein Serine-Threonine KinasesTBK1 protein, humanTbk1 protein, mouseInnate immunityNQO1TBK1Virus infection

Identifiers

PMID41913215
PMCPMC13159273

What OpenQuestion holds

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Registered trials

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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.