Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Combined Automated Annotation using Multiple IEA Methods
The Unc93b1 mutation 3d disrupts exogenous antigen presentation and signaling via Toll-like receptors 3, 7 and 9.
Assessing the function of human UNC-93B in Toll-like receptor signaling and major histocompatibility complex II response.
UNC93B1 delivers nucleotide-sensing toll-like receptors to endolysosomes.
IRAK-4- and MyD88-dependent pathways are essential for the removal of developing autoreactive B cells in humans.
BAD-LAMP is a novel biomarker of nonactivated human plasmacytoid dendritic cells.
UNC93B1 physically associates with human TLR8 and regulates TLR8-mediated signaling.
UNC93B1 is essential for the plasma membrane localization and signaling of Toll-like receptor 5.
A protein-interaction network of interferon-stimulated genes extends the innate immune system landscape.
A reference map of the human binary protein interactome.
Cryo-EM structures of Toll-like receptors in complex with UNC93B1.
Multilevel proteomics reveals host perturbations by SARS-CoV-2 and SARS-CoV.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
UNC93B1 attenuates the cGAS-STING signaling pathway by targeting STING for autophagy-lysosome degradation.
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UNC93B1 interacts with STING and promotes its autophagy-lysosome degradation in a trafficking-dependent manner, attenuating cGAS-STING-induced IFN-beta responses.
"UNC93B1 interacts with STING and suppresses STING-activated downstream signaling by delivering STING to the lysosomes for degradation, depending on its trafficking capability"
Large-scale mutational analysis identifies UNC93B1 variants that drive TLR-mediated autoimmunity in mice and humans.
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Alanine-scanning of UNC93B1 identifies positive and negative regulatory regions for TLR3, TLR7 and TLR9; heterozygous human T93I and R336C variants in negative regulatory regions enhance TLR7/8 responses and cause autoimmune/inflammatory disease.
"identified both negative and positive regulatory regions affecting TLR3, TLR7, and TLR9 responses"
Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus.
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Rare UNC93B1 missense variants cause SLE or chilblain lupus with differential gain of TLR7 and TLR8 activity.
"these observations suggest that UNC93B1 mutations cause monogenic SLE or CBL due to differentially enhanced TLR7 and TLR8 signaling"
Full-length TLR3/7/8/9 binds to UNC93B1
UNC93B1 delivers endosomal full-length TLRs to endolysosome
Endosomal TLRs pass through the Golgi
Defective UNC93B1 does not bind TLR3
Falcon deep research report on UNC93B1