The Unc93b1 mutation 3d disrupts exogenous antigen presentation and signaling via Toll-like receptors 3, 7 and 9
By K. Tabeta, K. Hoebe, E. Janssen, Xin Du, P. Georgel, K. Crozat, Suzanne Mudd, N. Mann, Sosathya Sovath, Jason Goode and 9 more. Nature Immunology, 2006
693 citations recorded by the source corpus.
Subfields: Endocrinology, Epidemiology, Immunology
View Paper: https://www.semanticscholar.org/paper/ecc54c44f4455688d57759986666ccac07086d08
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Citations in the corpus
- Plasmacytoid dendritic cells: sensing nucleic acids in viral infection and autoimmune diseases (2008, background): “The delivery of TLRs to endolysosomes and their subsequent proper activation requires UNC93B, an ER-resident transmembrane protein that can specifically interact with TLR3, TLR7 and TLR9 (Ref”
- Pattern recognition receptors and inflammation. (2010, background): “…into the nucleus to induce expression of type I IFN genes. revealed that UNC93B1 (an ER protein with 12 membrane-spanning domains) is responsible for TLR3, TLR7, and TLR9 signaling by governing the translocation of these TLRs from the ER to the endolysosome (Kim et al., 2008; Tabeta et al., 2006).”
- A cell biological view of Toll-like receptor function: regulation through compartmentalization (2009, background): “One notable exception to the typical nature of TLR7 and TLR9 trafficking is the requirement for UNC93B1 , a 12-membrane-spanning protein that resides in the E”
- Innate Immunity to Virus Infection (2009, background): “TLR7 and TLR9 from the ER to endosomes (83, 84).”
- The role of pattern-recognition receptors in innate immunity: update on Toll-like receptors (2010, background): “Triple D (3d) mice bearing a single missense mutation in the gene encoding UNC93B1 have defects in cytokine production and upregulation of costimulatory molecules in response to TLR7 and TLR9 ligands, as well as TLR3 ligands, and are highly susceptible to viral and bacterial infectio”