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Fig. 9 | Cell Communication and Signaling

Fig. 9

From: Amino acid response by Halofuginone in Cancer cells triggers autophagy through proteasome degradation of mTOR

Fig. 9

Schematic representation of the main findings of the study. Under normal conditions (left), mTORC1 is recruited on the membrane of the lysosomes and downregulates autophagy by inhibiting ULK1 complex. HF (right) triggers the Amino Acid starvation Response (AAR) by inhibiting the prolyl-tRNA synthetase and induces the detachment of mTORC1 from the lysosomes. As result, mTORC1 no longer inhibits ULK1, TFEB detaches from mTORC1 and relocates into the nucleus, and autophagy is induced. Following HF, mTOR is partially inactivated and degraded by the proteasome. Extra supplementation of proline rescues the induction of AAR, mTORC1 detachment from the lysosomes, mTOR degradation and autophagy induction

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Cell Communication and Signaling

ISSN: 1478-811X