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. 2021 Jun 18;8:697913. doi: 10.3389/fmolb.2021.697913

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Copyright © 2021 Dekker and Rüdiger.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Graphical abstract of the TRAP1 pathway. TRAP1 is transcribed by HSF1, which is deactivated by the HSP90 complex. PINK1 phosphorylation can activate TRAP1, whereas GzmM can cleave TRAP1, thereby hindering TRAP1 activity. Downstream of TRAP1, multiple pathways can influence mitochondrial function and cellular viability. FLTR:TRAP1 interactor PHB2 is inhibited, reducing mitophagy. Stalk construction can be mediated through TNFR1, via STAT3 phosphorylation, activation of transcription factor E2F1, which transcribes N-cadherin responsible for calcium regulation and cell adhesion. Through inhibition of CypD, TRAP1 can prevent mitochondrial pore opening and release of Cyt c to the cytosol, which is critical in the prevention of apoptosis. TRAP1 can influence calcium regulation through Sorcin, which is essential to keep the mitochondrial pores close. By inhibiting c-Scr, TRAP1 acts as a metabolic switch, which results in less ROS production. In association with TBP7 on the ER, TRAP1 can influence calcium regulation between the mitochondria and ER. Together with HSP90, TRAP1 is involved in inhibition of the unfolded protein response and promoting cell survival. Figure made with BioRender.