Figure 7
Model of Atg7-mediated AML chemoresistance. Chemotherapy exerts ER stress/genotoxic stress, and cell fate depends on the type of cells. If they are Atg7+/+ cells, stress might be mitigated with autophagy to inhibit apoptosis. However, if they are Atg7−/− cells, stress will lead to an increase in Noxa and a decrease in its counterpart Mcl-1, resetting apoptosis regulation at the mitochondrial outer membrane to induce the mitochondrial-mediated pathway of cell death.

Model of Atg7-mediated AML chemoresistance. Chemotherapy exerts ER stress/genotoxic stress, and cell fate depends on the type of cells. If they are Atg7+/+ cells, stress might be mitigated with autophagy to inhibit apoptosis. However, if they are Atg7−/− cells, stress will lead to an increase in Noxa and a decrease in its counterpart Mcl-1, resetting apoptosis regulation at the mitochondrial outer membrane to induce the mitochondrial-mediated pathway of cell death.

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