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. 2021 Jan 23;11(7):1835–1852. doi: 10.1016/j.apsb.2021.01.015

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© 2021 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig. 8 — Schematic illustration of CP-25 improves EP4 desensitization mediated FLS dysfunction via stabilizing KD and controlling Ala321 of GRK2. PGE2 level in FLS of CIA rats was up-regulated, promoting PGE2 binding to the EP4 receptor, inducing the increasing of GRK2 translocation, leading to EP4 over-desensitization, thereby promoting FLS dysfunction. CP-25 can stabilize the kinase domain of GRK2 to directly inhibit GRK2 kinase, leading to decreasing of GRK2 translocation to EP4 by controlling Ala321 of GRK2, thereby promoting EP4 resensitization, which was an important mechanism of CP-25 in improving FLS dysfunction.