ArticlePLoS pathogens2026
SARS-CoV-2 Nsp1 suppresses the canonical NF-κB pathway by promoting ubiquitin-dependent degradation of TAK1 kinase.
Article in PLoS pathogens, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Targeting the nuclear factor kappa B pathway for the medical management of intervertebral disc degeneration.Frontiers in neuroscience · 2026Review
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Authors and funding
14 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Immunoregulatory proteins expressed by SARS-CoV-2 interfere with host antiviral defences in infected cells and play critical roles in the pathogenesis and clinical manifestations of COVID-19. Here, we established a prediction algorithm by integrating a pretrained protein-language model and gene weights in immune-related pathways to quantify perturbations of SARS-CoV-2 proteins in host immunity. The results revealed that the canonical NF-κB pathway was dynamically regulated by SARS-CoV-2 infection and that nonstructural protein 1 (Nsp1) significantly suppressed the activation of the NF-κB pathway by other viral proteins and proinflammatory cytokines, such as IL-1β. Nsp1 binds to TAK1 at the TAB1-binding domain, promoting TRIM21-mediated K48-linked ubiquitination and subsequent proteasomal protein degradation, leading to the inactivation of the NF-κB signalling pathway. This work presents a novel framework to identify viral immunoregulators at the pathway level and provides mechanistic insights into immune evasion by SARS-CoV-2.
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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.