| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 1mg | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
Cell lines | 3T3-Swiss Albino cells |
Preparation method | The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below - 20 ℃ for several months. |
Reacting condition | 25 μM; 24 hrs |
Applications | In zinc-deficient 3T3-Swiss Albino cells, Z-DQMD-FMK (25 μM) prevented activation of caspase-3. Z-DQMD-FMK treatment did not restore cell number, but resulted in processing of full-length PKC-δ to a 56-kDa fragment. |
| 产品描述 | 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. References: |
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