ArticleJournal of virology2023
Cytokine Receptor-Like Factor 3 Negatively Regulates Antiviral Immunity by Promoting the Degradation of TBK1 in Teleost Fish.
Article in Journal of virology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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.
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.
Who cites it
13 citing papers in PubMed, 33 citations in OpenAlex.
- Fish CDK2 recruits Dtx4 to degrade TBK1 through ubiquitination in the antiviral response.eLife · 2026Article
- Expressional and prognostic value of cytokine receptor-like factor 3 in liver hepatocellular carcinoma patients via integrated bioinformatics analyses and experiments.SAGE open medicine · 2026Article
- Multiple Mammalian Cytokines and Erythropoietin-Mimetic Peptides Protect Insect Neurons via Phylogenetically Conserved Cytokine Receptor-Like Factor 3 (CRLF3).Journal of neurochemistry · 2025Article
- Mechanisms of CRLF3-targeted binding to ACTR2 to promote hepatocellular carcinoma progression and effects on the immune microenvironment.Cytotechnology · 2025Article
- Cytokine Receptor-like Factor 3 (CRLF3) and Its Emerging Roles in Neurobiology, Hematopoiesis and Related Human Diseases.International journal of molecular sciences · 2025Review
- RNA-Seq analysis reveals the long noncoding RNAs associated with immunity in wild Myotis myotis bats.BMC genomics · 2025Article
- Correlation between large rearrangements and patient phenotypes in NF1 deletion syndrome: an update and review.BMC medical genomics · 2024Article
- EFHD2 cooperates with E3 ubiquitin ligase Smurf1 to facilitate virus infection by promoting the degradation of TRAF6 in teleost fish.Journal of virology · 2024Article
- Identification of TBK1 inhibitors against breast cancer using a computational approach supported by machine learning.Frontiers in pharmacology · 2024Article
- A common single nucleotide variant in the cytokine receptor-like factor-3 (CRLF3) gene causes neuronal deficits in human and mouse cells.Human molecular genetics · 2023Article
- circMORC3-encoded novel protein negatively regulates antiviral immunity through synergizing with host gene MORC3.PLoS pathogens · 2023Article
- Smyd3 negatively regulates the anti-viral pathway by promoting TAK1 degradation in teleost fish.Journal of virology · 2023Article
- A novel protein encoded by circVPS13D attenuates antiviral innate immunity by targeting MAVS in teleost fish.Journal of virology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cytokine receptor-like factor 3 (Crlf3) belongs to the orphan class I cytokine receptors and is identified as a neuroprotective erythropoietin receptor. In previous studies of Crlf3, few focused on its role in innate immunity. Therefore, this study explored the regulatory role of Crlf3 in innate immunity. TANK-binding kinase 1 (TBK1) is a vital adaptor protein for the activation of the RLRs-MVAS-IRF3 antiviral signaling axis; thus, its expression and activity must be tightly regulated to maintain immune homeostasis and avoid undesirable effects. Here, we report that Crlf3 is a negative regulator of type I interferon production. The expression of Crlf3 is induced by poly(I·C) or Siniperca chuatsi rhabdovirus (SCRV) treatment. Silencing of Crlf3 enhanced poly(I·C)- and SCRV-induced type I interferon production, whereas overexpression of Crlf3 suppressed type I interferon production. Mechanistically, Crlf3 interacted with TBK1 via its N domain and then inhibited type I interferon production by promoting TBK1 proteasomal degradation through K48-linked polyubiquitination. Our study shows that Crlf3 is a key factor for viral escape from innate antiviral immunity in fish and provides a new perspective on mammalian resistance to viral invasion.
Indexed as
Identifiers
What OpenQuestion holds
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.