Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
A reverse genetic analysis of components of the Toll signaling pathway in Caenorhabditis elegans.
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Only tol-1, of tol-1, trf-1, pik-1 and ikb-1, is required for development; none is important for resistance to several pathogens; tol-1 mutants fail to avoid Serratia marcescens.
A conserved Toll-like receptor is required for Caenorhabditis elegans innate immunity.
Toll-like Receptor Signaling Promotes Development and Function of Sensory Neurons Required for a C. elegans Pathogen-Avoidance Behavior.
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TOL-1 acts cell-specifically in BAG neurons with TRF-1 and PIK-1, upstream of PMK-3, to promote BAG gene expression and CO2 sensing, which is required for avoidance of Serratia marcescens; ikb-1 deletion suppresses the tol-1 defect.
Structural basis and functional roles for Toll-like receptor binding to Latrophilin in C. elegans development.
Toll-like receptor signaling in neurons modulates C. elegans feeding behavior in a hunger state-dependent manner.
Toll-like receptor homolog TOL-1 regulates Bifidobacterium infantis-elicited longevity and behavior in Caenorhabditis elegans.
Lactobacillus casei triggers a TLR mediated RACK-1 dependent p38 MAPK pathway in Caenorhabditis elegans to resist Klebsiella pneumoniae infection.
MyD88-deficient Hydra reveal an ancient function of TLR signaling in sensing bacterial colonizers.
Sea anemone model has a single Toll-like receptor that can function in pathogen detection, NF-κB signal transduction, and development.