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In this model, the E3 ligase tumor necrosis factor receptor-associated factor 6 (TRAF6) promotes k63-linked ubiquitination of krϋppel-like transcription factor 5 (KLF5) and facilitates the interaction of KLF5 with downstream molecules, which provides a new possibility for a therapeutic approach to MsPGN[10]
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Agonists typically stabilize the active conformation of the receptor, promoting G protein coupling, while antagonists stabilize the inactive state or prevent activation-associated conformational changes 72 (Fig
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