Associated Papers
Identification of a novel TLR7 gain-of-function variant that underlies systemic lupus erythematosus.
Sethumadhavan A et al.
Journal of Human Immunity, 2026
Large-scale mutational analysis identifies UNC93B1 variants that drive TLR-mediated autoimmunity in mice and humans.
Rael VE et al.
The Journal of Experimental Medicine, 2024
Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus.
David C et al.
The Journal of Experimental Medicine, 2024
Human and Murine Toll-like Receptor-Driven Disease in Systemic Lupus Erythematosus.
von Hofsten S et al.
International Journal of Molecular Sciences, 2024
Disrupted degradative sorting of TLR7 is associated with human lupus.
Mishra H et al.
Science Immunology, 2024
UNC93B1 variants underlie TLR7-dependent autoimmunity.
Wolf C et al.
Science Immunology, 2024
N-glycosylation of UNC93B1 at a Specific Asparagine Residue Is Required for TLR9 Signaling.
Song HS et al.
Frontiers in Immunology, 2022
Cryo-EM structures of Toll-like receptors in complex with UNC93B1.
Ishida H et al.
Nature Structural & Molecular Biology, 2021
The ectodomain of TLR3 receptor is required for its plasma membrane translocation.
Pohar J et al.
Plos One, 2014
Acidic amino acid residues in the juxtamembrane region of the nucleotide-sensing TLRs are important for UNC93B1 binding and signaling.
Kim J et al.
Journal of Immunology (baltimore, Md. : 1950), 2013
An ENU-induced splicing mutation reveals a role for Unc93b1 in early immune cell activation following influenza A H1N1 infection.
Lafferty EI et al.
Genes and Immunity, 0
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