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Notably, CB-839 caused an increase of MCL-1 protein expression in the CLL cell lines, but the cells BCL-2 expression remained stable

1c,d) and was previously suggested as a candidate for a potential activator site, first, because its positive charge might stabilize or bind GSH as GS , and, second, because of its evolutionary conserved position that is equivalent to the GSH-interacting catalytic residue of glutathione transferases 3

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Similar to the effects observed with E protein expression, MHV infection elicited a dose-dependent release of mIL1 in HEK293T cells expressing the MHV receptor mCC1a (Fig