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Conclusions Taken together, the development of pharmacological molecules that elevate endogenous Rab7 activity via inhibition of TBC1D15-mediated Rab7 inactivation could be beneficial in NPC1 disease and other neurological disorders with endolysosomal dysfunction, and allow advances to better understand how Rab7- and TBC1D15-related activities contribute to Charcot-Marie-Tooth type 2B and lysosome regeneration in neurodegeneration [87, 90,91,92,93,94]

It is worth noting that several amino acid transporters, such as SNAT2, SNAT9, and PAT4 are considered transceptors and shown to regulate mTORC1 independent of their transport function 54,55

As a result, antioxidants may be used in combination with other treatments for UC

Meier DT, Rachid L, Wiedemann SJ et al (2022) Prohormone convertase 1/3 deficiency causes obesity due to impaired proinsulin processing