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anti-Human UNC93B1 Antibodies:
anti-Mouse (Murine) UNC93B1 Antibodies:
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Human Polyclonal UNC93B1 Primary Antibody for IHC, ELISA - ABIN1003411
Brinkmann, Spooner, Hoebe, Beutler, Ploegh, Kim: The interaction between the ER membrane protein UNC93B and TLR3, 7, and 9 is crucial for TLR signaling. in The Journal of cell biology 2007
Show all 2 Pubmed References
Human Polyclonal UNC93B1 Primary Antibody for WB - ABIN4364376
Nakano, Morimoto, Suzuki, Watanabe, Amano, Takasaki: Up-regulation of the endoplasmic reticulum transmembrane protein UNC93B in the B cells of patients with active systemic lupus erythematosus. in Rheumatology (Oxford, England) 2010
Show all 2 Pubmed References
Endosomal localization of endogenous TLR3 (show TLR3 Antibodies) 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 Antibodies)(+) but not switched B cells were strongly reduced in MYD88 (show MYD88 Antibodies)-, IRAK-4 (show IRAK4 Antibodies)-, and TIRAP (show TIRAP Antibodies)-deficient patients, but not UNC-93B-deficient patients.
TLR3 (show TLR3 Antibodies) is the important regulator of UNC93B1 that in turn governs the responsiveness of all TLR3 (show TLR3 Antibodies) as the important regulator of UNC93B1 that in turn governs the responsiveness of all NAS (show SCN9A Antibodies) Toll (show TLR4 Antibodies)-like receptors
UNC93B1 expression is required for TLR3 (show TLR3 Antibodies) cleavage and signaling.
UNC93B1 physically associates with human TLR8 (show TLR8 Antibodies) and regulates TLR8 (show TLR8 Antibodies)-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 Antibodies) UNC-93B, resulting in impaired cellular interferon-alpha (show IFNA Antibodies)/beta and -lambda antiviral responses
No UNC-93B1 mutations were foundin patients with MRS.
IRAK-4 (show IRAK4 Antibodies)-, MyD88 (show MYD88 Antibodies)-, and UNC-93B-deficient patients did not display autoreactive antibodies in their serum or develop autoimmune diseases, suggesting that IRAK-4 (show IRAK4 Antibodies), MyD88 (show MYD88 Antibodies), and UNC-93B pathway blockade may thwart autoimmunity in humans.
regulates ligand-induced trafficking of TLR7 (show TLR7 Antibodies) and TLR9 (show TLR9 Antibodies) from the ER to endolysosomes, potential therapeutic target for controlling dysregulated TLR7 (show TLR7 Antibodies)/9 responses in autoimmune diseases
autoantibody production in systemic mercury-induced autoimmunity was dependent on the endosomal TLR transporter UNC93B1
Autophagy contributes to macrophage resistance to Leishmania major. Data, including data from studies in knockout mice, suggest a key resistance mechanism involves endosomal signaling via Tlr3 (show TLR3 Antibodies)/7/9 in macrophages; macrophages deficient for Tlr3 (show TLR3 Antibodies)/7/9, Unc93b1, or MyD88 (show MYD88 Antibodies) fail to undergo L. major-induced autophagy. (TLR = Toll (show TLR4 Antibodies)-like receptor; Unc93b1 = unc-93 homolog B1; MyD88 (show MYD88 Antibodies) = myeloid differentiation primary response gene 88 (show MYD88 Antibodies))
Describe a mechanism for differential sorting of endosomal toll (show TLR4 Antibodies) 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 Antibodies), a cell surface receptor for bacterial protein flagellin (show FliC Antibodies), also requires UNC93B1 for plasma membrane localization and signaling.
The observations demonstrate for the first time that activation of interferon (show IFNA Antibodies) and estrogen signaling in immune cells up-regulates the expression of murine Unc93b1.
Mutation of the acidic residues in TLR3 (show TLR3 Antibodies) and TLR9 (show TLR9 Antibodies) 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 Antibodies)/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.
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