ArticleiScience2025
The PYRIN domain is required for TLR4-mediated inflammation by PYHIN family members.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
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Who cites it
4 citing papers in PubMed.
- SMAD7-Associated Glycolytic Regulation Promotes Lactate-Dependent Macrophage Phenotype Modulation in Colorectal Cancer.Cancers · 2026Article
- Analysis and validation of abnormal signaling pathways and immune cell infiltration characteristics in digestive system cancers based on peroxisome-related genes.Biology direct · 2026Article
- The impact of hypoxia and glycolysis on liver fibrosis.Journal of translational medicine · 2026Article
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Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Innate immunity relies on pattern recognition receptors (PRRs) to detect threats, including pathogens and damage-associated molecular patterns (DAMPs) from damaged cells. IFI16 behaves as a DAMP and activates Toll-like receptor 4 (TLR4)-mediated inflammation. Here, we identify the N-terminal PYRIN domain (PYD) of IFI16 as critical for binding TLR4 and triggering inflammation, and we confirm this interaction through
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Registered trials
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