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anti-Human UNC93B1 Antikörper:
anti-Mouse (Murine) UNC93B1 Antikörper:
anti-Rat (Rattus) UNC93B1 Antikörper:
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Human Polyclonal UNC93B1 Primary Antibody für IHC (p), WB - ABIN541343
Tabeta, Hoebe, Janssen, Du, Georgel, Crozat, Mudd, Mann, Sovath, Goode, Shamel, Herskovits, Portnoy, Cooke, Tarantino, Wiltshire, Steinberg, Grinstein, Beutler: The Unc93b1 mutation 3d disrupts exogenous antigen presentation and signaling via Toll-like receptors 3, 7 and 9. in Nature immunology 2006
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Human Polyclonal UNC93B1 Primary Antibody für 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
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Human Polyclonal UNC93B1 Primary Antibody für 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
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Our results suggest that rare protein-altering variants in the C10orf88 and UNC93B1 genes are associated with a worse response to anti-VEGF therapy in patients with neovascular age-related macular degeneration, but these results require further validation in other cohorts.
Expression of a constitutively active STIM1 mutant, which no longer binds UNC93B1, restores antigen degradation and cross-presentation in 3d-mutated dendritic cells.
Endosomal localization of endogenous TLR3 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(+) but not switched B cells were strongly reduced in MYD88-, IRAK-4-, and TIRAP-deficient patients, but not UNC-93B-deficient patients.
TLR3 is the important regulator of UNC93B1 that in turn governs the responsiveness of all TLR3 as the important regulator of UNC93B1 that in turn governs the responsiveness of all NAS Toll-like receptors
UNC93B1 expression is required for TLR3 cleavage and signaling.
UNC93B1 physically associates with human TLR8 and regulates TLR8-mediated signaling
To date only 2 children with UNC-93B deficiencies have been identified after isolated HSV-1 encephalitis.
Haplotype H3 of the hUNC-93B1 gene seems related to E/A-ratio in elderly men. The relationship between the hUNC-93B1 gene and the age at onset of heart failure and mortality support a view of a clinically relevant impact of the gene.
findings elucidate a genetic etiology for herpes simplex virus encephalitis in two children with autosomal recessive deficiency in the intracellular protein UNC-93B, resulting in impaired cellular interferon-alpha/beta and -lambda antiviral responses
study confirms the function of UNC-93B for innate immunity in human beings, and extends the knowledge for this molecule to the analysis of its regulation and the subcellular localization of the endogenous protein
No UNC-93B1 mutations were foundin patients with MRS.
IRAK-4-, MyD88-, and UNC-93B-deficient patients did not display autoreactive antibodies in their serum or develop autoimmune diseases, suggesting that IRAK-4, MyD88, and UNC-93B pathway blockade may thwart autoimmunity in humans.
regulates ligand-induced trafficking of TLR7 and TLR9 from the ER to endolysosomes, potential therapeutic target for controlling dysregulated TLR7/9 responses in autoimmune diseases
Individuals with congenital mutations develop severe HSV-1 encephalitis
Data show that Unc-93 homolog B1 (UNC93B1) is critical for maintaining Toll-like receptors (TLRs) expression.
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 Tlr3/7/9 in macrophages; macrophages deficient for Tlr3/7/9, Unc93b1, or MyD88 fail to undergo L. major-induced autophagy. (TLR = Toll-like receptor; Unc93b1 = unc-93 homolog B1; MyD88 = myeloid differentiation primary response gene 88)
Describe a mechanism for differential sorting of endosomal toll 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, a cell surface receptor for bacterial protein flagellin, also requires UNC93B1 for plasma membrane localization and signaling.
The observations demonstrate for the first time that activation of interferon and estrogen signaling in immune cells up-regulates the expression of murine Unc93b1.
Mutation of the acidic residues in TLR3 and TLR9 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 TLR3/7/9 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-like receptors 3, 7, and 9, is required for bacterial RNA-induced IL-1beta production and activation of caspase-1.
restricts systemic lethal inflammation by orchestrating Toll-like receptor 7 and 9 trafficking
association with UNC93B1 and the intracellular localization of TLRs are not unique features of nucleic acid-sensing TLRs but is also essential for TLR11-dependent recognition of T. gondii profilin and for host protection against this parasite.
our results reveal a critical role for UNC93B1 on induction of IL-12/IFNgamma production as well as autonomous control of Toxoplasma replication by macrophages.
identified 'triple D' (3d), a recessive N-ethyl-N-nitrosourea-induced mutation and phenotype in which no signaling occurs via the intracellular Toll-like receptors 3, 7 and 9
Study shows that UNC93B specifically interacts with TLR3, 7, 9, and 13, whereas introduction of the point mutation H412R in UNC93B abolishes their interactions.
the function of the polytopic membrane protein UNC93B1 is to deliver the nucleotide-sensing receptors TLR7 and TLR9 from the ER to endolysosomes
Data suggest that the Toll-like receptor 7/9 response to nucleic acids in dendritic cells is biased toward DNA-sensing by Unc93B1.
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