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- W1554871497 abstract "The seven transmembrane G protein‐coupled receptor E pstein‐ B arr virus ( EBV ) induced gene 2 ( EB I2; also known as GPR 183) was identified in 1993 on the basis of its substantial upregulation in EBV ‐infected cells. It is primarily expressed in lymphoid cells; most abundantly in B cells. EBI 2 is central for the positioning of B cells within the lymphoid organs, a process that is regulated in part by a chemotactic gradient formed by the endogenous lipid agonists, and in part by a fine‐tuned regulation of EBI 2 cell surface expression. The most potent endogenous EBI 2 agonist is 7α, 25‐dihydroxyxcholesterol (7α,25‐ OHC ), yet many structurally related oxysterols can bind to an EBI 2 pocket that is defined by the upper parts of the transmembrane helices and extracellular receptor regions. EBI 2 signals via Gαi, as well as via G protein‐independent pathways like β‐arrestin recruitment. The concerted action of these pathways leads to cell migration. By genetically interfering with its up‐ and downregulation, EBI 2 was also recently shown to induce cell proliferation, an action that could be inhibited by small molecule antagonists. Here, we focus on the oxysterol– EBI 2 axis in immune control, including its role in the EBV life cycle. We also summarize the structural and functional properties of EBI 2 interaction with oxysterol agonists and small molecule antagonists and discuss EBI 2 as therapeutic target for diseases of the immune system." @default.
- W1554871497 created "2016-06-24" @default.
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- W1554871497 date "2014-06-20" @default.
- W1554871497 modified "2023-10-16" @default.
- W1554871497 title "Oxysterol‐EBI2 signaling in immune regulation and viral infection" @default.
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- W1554871497 doi "https://doi.org/10.1002/eji.201444493" @default.
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