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Description

Schroll, A

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Genetic and pharmacologic ABCC1 inactivation potentiates the anti-leukemic effects of BCL-2 inhibitors and efficiently re-sensitizes Venetoclax-resistant leukemia cells

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N-Acetyl Cysteine (NAC) provides the rate-limiting amino acid cysteine for endogenous glutathione synthesis and has been described as a safe intervention for glutathione deficiency (Atkuri et al., 2007)

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Cellular redox homeostasis is an essential buffering mechanism that prevents exces- sive reduction or oxidation

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