ReviewImmunology2026
MyD88-Family Adaptors: Compartmentalised Signalling and Non-Immune Functions.
Review in Immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
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Authors and funding
7 authors.
Funding
Abstract
The myeloid differentiation primary response protein 88 (MyD88) family of Toll/interleukin-1 receptor (TIR) domain-containing adaptor proteins constitutes a central signalling hub that integrates innate immune sensing with tissue-specific stress responses. This family comprises five mammalian members: MyD88, TIRAP/MAL, TRIF/TICAM-1, TRAM/TICAM-2 and SARM1 (also known as MyD88-1 through MyD88-5). While these adaptors are classically defined by their roles in immune and haematopoietic cells, accumulating genetic and mechanistic evidence demonstrates critical, cell-intrinsic functions in non-immune tissues. Canonical MyD88 signalling assembles IRAK-containing complexes to activate NF-κB and MAPK pathways, whereas TIRAP and TRAM function as sorting adaptors that impose spatial and receptor specificity. TRIF mediates MyD88-independent interferon programs downstream of Toll-like receptor (TLR)-3 and internalised TLR-4. Beyond immunity, MyD88-family signalling regulates epithelial barrier integrity, hepatic metabolic homeostasis, skeletal muscle metabolism and atrophy, endothelial permeability, renal injury responses and neuronal degeneration. Notably, SARM1 represents a functionally divergent family member whose TIR domain acts as an intrinsic NAD
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