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Endosomal localization of endogenous TLR3 (show TLR3 ELISA Kits) was decreased by silencing of LRRC59, suggesting that LRRC59 promotes UNC93B1-mediated translocation of NA-sensing TLRs from the ER upon infection.
the UNC93B1 tyrosine-based motif regulates trafficking and TLR responses via separate mechanisms.
IgM(+)IgD(+)CD27 (show CD27 ELISA Kits)(+) but not switched B cells were strongly reduced in MYD88 (show MYD88 ELISA Kits)-, IRAK-4 (show IRAK4 ELISA Kits)-, and TIRAP (show TIRAP ELISA Kits)-deficient patients, but not UNC-93B-deficient patients.
TLR3 (show TLR3 ELISA Kits) is the important regulator of UNC93B1 that in turn governs the responsiveness of all TLR3 (show TLR3 ELISA Kits) as the important regulator of UNC93B1 that in turn governs the responsiveness of all NAS (show SCN9A ELISA Kits) Toll (show TLR4 ELISA Kits)-like receptors
UNC93B1 expression is required for TLR3 (show TLR3 ELISA Kits) cleavage and signaling.
UNC93B1 physically associates with human TLR8 (show TLR8 ELISA Kits) and regulates TLR8 (show TLR8 ELISA Kits)-mediated signaling
findings elucidate a genetic etiology for herpes simplex virus encephalitis in two children with autosomal recessive deficiency in the intracellular protein (show CKAP2 ELISA Kits) UNC-93B, resulting in impaired cellular interferon-alpha (show IFNA ELISA Kits)/beta and -lambda antiviral responses
No UNC-93B1 mutations were foundin patients with MRS.
IRAK-4 (show IRAK4 ELISA Kits)-, MyD88 (show MYD88 ELISA Kits)-, and UNC-93B-deficient patients did not display autoreactive antibodies in their serum or develop autoimmune diseases, suggesting that IRAK-4 (show IRAK4 ELISA Kits), MyD88 (show MYD88 ELISA Kits), and UNC-93B pathway blockade may thwart autoimmunity in humans.
regulates ligand-induced trafficking of TLR7 (show TLR7 ELISA Kits) and TLR9 (show TLR9 ELISA Kits) from the ER to endolysosomes, potential therapeutic target for controlling dysregulated TLR7 (show TLR7 ELISA Kits)/9 responses in autoimmune diseases
Describe a mechanism for differential sorting of endosomal toll (show TLR4 ELISA Kits) like receptors by UNC93B1.
These observations establish a significant role for Unc93b1 in the regulation of the host inflammatory response to CVB3 infection and also reveal potential mediators of host tissue damage that merit further investigation in acute viral myocarditis.
Unc93b1 controls activation of both myeloid and lymphoid cells during the innate immune response to influenza.
We discovered that TLR5 (show TLR5 ELISA Kits), a cell surface receptor for bacterial protein flagellin (show FliC ELISA Kits), also requires UNC93B1 for plasma membrane localization and signaling.
The observations demonstrate for the first time that activation of interferon (show IFNA ELISA Kits) and estrogen signaling in immune cells up-regulates the expression of murine Unc93b1.
Mutation of the acidic residues in TLR3 (show TLR3 ELISA Kits) and TLR9 (show TLR9 ELISA Kits) prevents UNC93B1 binding, and impairs TLR trafficking and renders the mutant receptors incapable of transmitting signals; therefore, the acidic residues in the juxtamembrane region of the nucleotide-sensing TLRs have important functional roles
Data indicate that UNC93B1 mutant and triple TLR3 (show TLR3 ELISA Kits)/7/9 knock-out mice are highly susceptible to infection with Leishmania major.
UNC93B1 mediates innate inflammation and antiviral defense in the liver during acute murine cytomegalovirus infection.
UNC93B, but not Toll (show TLR4 ELISA Kits)-like receptors 3, 7, and 9, is required for bacterial RNA-induced IL-1beta (show IL1B ELISA Kits) production and activation of caspase-1 (show CASP1 ELISA Kits).
restricts systemic lethal inflammation by orchestrating Toll-like receptor 7 (show TLR7 ELISA Kits) and 9 trafficking
This gene encodes a protein with similarity to the C. elegans unc93 protein. The Unc93 protein is involved in the regulation or coordination of muscle contraction in the worm.
unc-93 homolog B1 (C. elegans)
, protein unc-93 homolog B1
, unc-93 related protein
, unc93 homolog B
, unc93 homolog B1
, unc-93 homolog B