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Schematic model of regulation of G2385R LRRK2 stability.
We propose that the G2385R substitution causes misfolding of LRRK2, thereby promoting CHIP-mediated proteasomal degradation. Such misfolding can be antagonized by Hsp90 as inhibition of Hsp90 binding by Geldanamycin shifts the equilibrium toward CHIP-dependent degradation of the protein.
