Fig. 11

A schematic representation of the molecular mechanisms regulating Hst1’s endocytosis, trafficking, targeting and promoting effect on cell metabolic activity. Hst1 binds to GPCR, is then taken up via clathrin-meditated endocytosis, and subsequently, the Hst1-containing EEs moved towards the center of the cell, interacted and disassociated with mitochondria, during which F-Hst1 was released to mitochondria. Hst1 increases mitochondria-ER contacts (MERCs), which may enable the transfer of Ca2+ from ER to mitochondria to enhance the cellular metabolic activity. The ER target protein S2R/TMEM97 of Hst1 also critically regulates the Hst1-stimulating cellular metabolic activity