gopubmed logo
 
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Unc-93 homolog B1

UNC93B1, UNC-93B, unc-93
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. [provided by RefSeq, Jul 2008] (from NCBI)
Sponsored links
Top mentioned proteins: TLR3, TLR9, TLR7, ACID, CAN
Papers using UNC93B1 antibodies
Identification of a polyI:C-inducible membrane protein that participates in dendritic cell-mediated natural killer cell activation.
Supplier
Gay Nick, In PLoS ONE, 2009
... mAb (Biolegend), anti-MPR pAb (Abcam, Cambridge, UK), anti-human TLR8 mAb (Dendritics, LYON, France) and anti-human UNC93B1 pAb (ProSci Inc., Poway, CA) ...
Papers on UNC93B1
Synergy between Hematopoietic and Radioresistant Stromal Cells Is Required for Autoimmune Manifestations of DNase II-/-IFNaR-/- Mice.
New
Marshak-Rothstein et al., Worcester, United States. In J Immunol, Feb 2016
UNASSIGNED: Detection of endogenous nucleic acids by cytosolic receptors, dependent on STING, and endosomal sensors, dependent on Unc93b1, can provoke inflammatory responses that contribute to a variety of autoimmune and autoinflammatory diseases.
Type I IFN Contributes to the Phenotype of Unc93b1D34A/D34A Mice by Regulating TLR7 Expression in B Cells and Dendritic Cells.
New
Miyake et al., Tokyo, Japan. In J Immunol, Feb 2016
Unc93 homolog B1 (Unc93B1) is a regulator of TLR7 that controls the TLR7 response by transporting TLR7 from the endoplasmic reticulum to endolysosomes.
Human TLR8 senses UR/URR motifs in bacterial and mitochondrial RNA.
New
Kirschning et al., Essen, Germany. In Embo Rep, Dec 2015
Moreover, Unc93b1(-/-)- and Tlr8(-/-)-THP-1 cells are refractory, while endogenous and ectopically expressed TLR8 confers responsiveness in a UR/URR RNA ligand consensus motif-dependent manner.
Guanosine and its modified derivatives are endogenous ligands for TLR7.
New
Miyake et al., Kawaguchi, Japan. In Int Immunol, Nov 2015
To address a role of G analogs in the disease state, we also examined macrophages from Unc93b1 (D34A/D34A) mice, which suffer from TLR7-dependent systemic inflammation, and found that Unc93b1 (D34A/D34A) macrophages showed significantly enhanced response to G alone or 8-OHdG with ORN.
[Clinical characteristics, prognosis and genetic susceptibility of herpes simplex encephalitis in children].
New
Liu et al., Beijing, China. In Zhonghua Er Ke Za Zhi, Sep 2015
OBJECTIVE: To summarize the clinical characteristics and long-term prognosis of herpes simplex virus encephalitis (HSE) in childhood and to analyze genotype of UNC93B1 and TLR3.
An unexpected role for RNA-sensing toll-like receptors in a murine model of DNA accrual.
Review
New
Marshak-Rothstein et al., Worcester, United States. In Clin Exp Rheumatol, Jul 2015
RESULTS: Mice that fail to express DNaseII, IFNaR, and Unc93b1 still develop arthritis but do not make autoantibodies, develop splenomegaly, or exhibit extramedullary haematopoiesis.
[Multilevel maturation of Toll-like receptor 9].
Review
Siednienko et al., Panama. In Postepy Hig Med Dosw (online), 2012
TLR9 delivery to the endosomes is mediated by two distinct proteins, UNC93B1 and AP-2, and post-early endosome distribution is determined by AP-3.
Mendelian predisposition to herpes simplex encephalitis.
Review
Casanova et al., New York City, United States. In Handb Clin Neurol, 2012
Autosomal recessive UNC-93B deficiency and autosomal dominant TLR3 deficiency were then described in children with isolated HSE.
Impaired intrinsic immunity to HSV-1 in human iPSC-derived TLR3-deficient CNS cells.
Impact
Notarangelo et al., New York City, United States. In Nature, 2012
We derived induced pluripotent stem cells (iPSCs) from the dermal fibroblasts of TLR3- and UNC-93B-deficient patients and from controls.
Dissecting immunity by germline mutagenesis.
Review
Rutschmann et al., London, United Kingdom. In Immunology, 2012
Mutations in previously uncharacterized genes in the mouse, like Unc93B or Themis, have demonstrated the impartiality of forward genetics and led to the identification of new crucial immunity actors.
Bacterial RNA mediates activation of caspase-1 and IL-1β release independently of TLRs 3, 7, 9 and TRIF but is dependent on UNC93B.
GeneRIF
Dalpke et al., Heidelberg, Germany. In J Immunol, 2012
UNC93B, but not Toll-like receptors 3, 7, and 9, is required for bacterial RNA-induced IL-1beta production and activation of caspase-1.
Cleavage of Toll-like receptor 3 by cathepsins B and H is essential for signaling.
GeneRIF
Benaroch et al., Paris, France. In Proc Natl Acad Sci U S A, 2012
UNC93B1 expression is required for TLR3 cleavage and signaling.
Inborn errors of anti-viral interferon immunity in humans.
Review
Casanova et al., Paris, France. In Curr Opin Virol, 2011
The narrow disorders impair exclusively (TLR3) or mostly (UNC-93B, TRIF, TRAF3) the TLR3-dependent induction of type I and III IFNs, leading to HSE in apparently otherwise healthy individuals.
Unc93B1 restricts systemic lethal inflammation by orchestrating Toll-like receptor 7 and 9 trafficking.
Impact
GeneRIF
Miyake et al., Tokyo, Japan. In Immunity, 2011
restricts systemic lethal inflammation by orchestrating Toll-like receptor 7 and 9 trafficking
Love triangle between Unc93B1, TLR7, and TLR9 prevents fatal attraction.
Impact
Iwasaki et al., New Haven, United States. In Immunity, 2011
Unc93B1, a multitransmembrane ER-resident protein, controls intracellular trafficking of endosomal Toll-like receptors.
Is it time to study TLR3 or UNC-93B pathway deficiencies in reactivated herpes simplex encephalitis?
GeneRIF
Gonzalez-Granado, In Pediatr Infect Dis J, 2011
To date only 2 children with UNC-93B deficiencies have been identified after isolated HSV-1 encephalitis.
UNC93B1 physically associates with human TLR8 and regulates TLR8-mediated signaling.
GeneRIF
Matsumoto et al., Sapporo, Japan. In Plos One, 2010
UNC93B1 physically associates with human TLR8 and regulates TLR8-mediated signaling
IRAK-4- and MyD88-dependent pathways are essential for the removal of developing autoreactive B cells in humans.
Impact
GeneRIF
Meffre et al., New York City, United States. In Immunity, 2008
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.
UNC93B1 delivers nucleotide-sensing toll-like receptors to endolysosomes.
Impact
GeneRIF
Ploegh et al., Cambridge, United States. In Nature, 2008
the function of the polytopic membrane protein UNC93B1 is to deliver the nucleotide-sensing receptors TLR7 and TLR9 from the ER to endolysosomes
share on facebooktweetadd +1mail to friends