ArticleJournal of cellular and molecular medicine2020
A mathematic model to reveal delicate cross-regulation between MAVS/STING, inflammasome and MyD88-dependent type I interferon signalling.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- Lumpy skin disease virus 001/156 protein is a virulence factor that suppresses interferon production through impairing IRF3 dimerization.PLoS pathogens · 2025Article
- Dual nature of type I interferon responses and feedback regulations by SOCS1 dictate malaria mortality.Journal of advanced research · 2025Article
- The contribution and mechanism of hypoxia/USP19/Beclin-1 feed-forward loop in cervical cancer.Biophysical journal · 2024Article
- High-resolution kinetic characterization of the RIG-I-signaling pathway and the antiviral response.Life science alliance · 2023Article
- Article
- The crosstalk between viral RNA- and DNA-sensing mechanisms.Cellular and molecular life sciences : CMLS · 2021Review
- A mathematic model to reveal delicate cross-regulation between MAVS/STING, inflammasome and MyD88-dependent type I interferon signalling.Journal of cellular and molecular medicine · 2020Article
- Accelerator or Brake: Immune Regulators in Malaria.Frontiers in cellular and infection microbiology · 2020Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Early type I interferon is essential for antagonizing against malaria infection, which remains a significant global infectious disease. After Plasmodium yoelii YM infection, the activation of MAVS-, STING- and inflammasome-IRF3-mediated pathway could trigger the Socs1 expression to inhibit the TLR7-MyD88-IRF7-induced type I interferon production. However, the dynamic regulatory mechanisms of type I interferon response to YM infection and delicate cross-regulation of these signalling are far from clear. In current study, we established a mathematical model to systematically demonstrate that the MAVS-, STING- and inflammasome-mediated signalling pathways play distinct roles in regulating type I interferon response after YM infection; and the YM dose could significantly affect the difference of resistance to YM infection among MAVS, STING and inflammasome deficiency. Collectively, our study systematically elucidated the precise regulatory mechanisms of type I interferon signalling after YM infection and advanced the research on therapy of plasmodium infection by incorporating multiple signalling pathways at diverse time.
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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.