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Small molecule antagonism of oxysterol-induced Epstein–Barr virus induced gene 2 (EBI2) activation

Authors
Journal
FEBS Open Bio
2211-5463
Publisher
Wiley Blackwell (John Wiley & Sons)
Volume
3
Identifiers
DOI: 10.1016/j.fob.2013.02.003
Keywords
  • 7Tm Receptors
  • Ebi2
  • Oxysterols
  • Antagonism
  • Map Kinase Activation
  • Epstein–Barr Virus
Disciplines
  • Biology
  • Medicine

Abstract

Abstract The Epstein–Barr virus induced gene 2 (EBI2) was recently identified as the first oxysterol-activated 7TM receptor. EBI2 is essential for B cell trafficking within lymphoid tissues and thus the humoral immune response in general. Here we characterize the antagonism of the non-peptide molecule GSK682753A, which blocks oxysterol-induced G-protein activation, β-arrestin recruitment and B-cell chemotaxis. We furthermore demonstrate that activation triggers pertussis toxin-sensitive MAP kinase phosphorylation, which is also inhibited by GSK682753A. Thus, EBI2 signalling in B cells mediates key phenotypic functions via signalling pathways amenable to manipulation providing additional therapeutic options for inhibiting EBI2 activity.

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