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Inhibition of caspase-3 processing by Z-DQMD-FMK (Z-Asp(OMe)-Gln-Met-Asp(OMe)-fluoromethylketone) did not restore cell number in the zinc-deficient group, but resulted in processing of full-length PKC-δ to a 56-kDa fragment1.

The inhibitory effect of specific caspase inhibitors (Z-DQMD-FMK, Z-IETD-FMK and Z-LEHD-FMK) suggests that the MG132-induced apoptotic cell death and depletion of GSH in SCLC cells are mediated by both activation of caspase-8 and mitochondrial damage, leading to the activation of caspase-9 and -32.

To investigate whether εPKC cleavage after stroke is caused by caspase-3 activation, we examined the effect of a cell-permeable caspase-3–specific inhibitor, Z-DQMD-FMK, on generation of cleaved εPKC fragments. Caspase-3 inhibition did not suppress the decrease in fulllength εPKC and the 43-kDa fragment in the ischemic core and penumbra after stroke3.

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