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Bellodi C et al (2009) Targeting autophagy potentiates tyrosine kinase inhibitor-induced cell death in Philadelphia chromosome-positive cells, including primary CML stem cells

A long, fragile peptide with no dedicated stabilization strategy does not become oral just by pressing it into a tablet

In summary, the hydroxyl group of the conserved active-site tyrosine residue is dispensable for the GSH-dependent reduction of GSSCys and does not play a general role as a GSH activator

Abstract The ability to generate and regulate energy, maintain metabolic flux, and preserve redox homeostasis is the basis of all cellular processes in both healthy and diseased tissues