Autophagy activator that upregulates lysosomal v-ATPase activity and induces its decoupling from Rag GTPases by covalently targeting v-ATPase subunit ATP6V1A Cys277.
EN6 is an autophagy activator that simultaneously upregulates lysosomal vacuolar H(+)-ATPase (v-ATPase) activity and induces its decoupling from the Rag GTPases by covalently targeting v-ATPase subunit ATP6V1A Cys277. EN6 blocks mTORC1 lysosomal recruitment & activation (1-4 hr 25 μM EN6 pretreatment prior to 10-min amino acids (AA) stimulation of AA-starived HEK293) and clears cellular TDP-43 aggregates (25 μM; U2OS with inducible TDP-43). When administered in mice in vivo (50 mg/kg ip.), EN6 inhibits mTORC1 signaling and activates autophagy in both skeletal muscle and heart tissue. Unlike bafilomycin A1 (BafA1), EN6 activates, but not inhibits v-ATPase catalytic activity.
Nature chemical biology, 15(8), 776-785 (2019-07-10)
Autophagy is a lysosomal degradation pathway that eliminates aggregated proteins and damaged organelles to maintain cellular homeostasis. A major route for activating autophagy involves inhibition of the mTORC1 kinase, but current mTORC1-targeting compounds do not allow complete and selective mTORC1
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