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In addition to common membrane repair mechanisms, such as the endosomal sorting complex needed for transport-III [72, 73], various antioxidant enzymes or proteins play a context-dependent role in selectively inhibiting oxidative cell death in cancer cells

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204 Similarly, administration of the PRMT5 inhibitor PJ-68 in a CML mouse model with high expression of PRMT5 LSCs could deplete DVL3, thereby inhibiting Wnt/-catenin signaling and significantly prolonging the survival time of a retroviral BCR-ABL-driven CML mouse model

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