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Given that M-cells have well-accepted BT capability and overlie intestinal lymphoid aggregates, M-cell mediated BT is one plausible mechanistic explanation [16, 17]

Although reactive electrophiles such as chloroacetamides are generally considered to be promiscuous in target binding, we demonstrated here using a BODIPY-labelled analogue that the chloroacetamide-based GSTO1 inhibitor C1-27 exhibited a low degree of nonspecific reactivity

Furthermore, 3-mercaptopyruvate sulfurtransferase-derived mitochondrial H2S may play a regulatory role in BCAA catabolism and mediate critical cardiovascular protection in heart failure (74)

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