Search results for: Caspase 10 Substrate AEVD pNA1000 assays
#20162409 
2010/02/17
To Up
Magnolol induces apoptosis via activation of both mitochondrial and death receptor pathways in A375-S2 cells.
Magnolol inhibited proliferation of human malignant melanoma A375-S2 cells. The drug induced oligonucleosomal fragmentation of DNA in A375-S2 cells and increased caspase-3, 8, 9 activities followed by the degradation of caspase-3 substrates, inhibitor of caspase dependent DNase (ICAD) and poly-(ADP-ribose) polymerase (PARP). Pan-caspase inhibitor (z-VADfmk), caspase-3 inhibitor (z-DEVD-fmk), capase-8 inhibitor (z-IETD-fmk), caspase-9 inhibitor (z-LEHD-fmk) and caspase-10 inhibitor (z-AEVD-fmk) inhibited magnolol-induced A375-S2 cell apoptosis. The level of anti-apoptotic mitochondrial protein Bcl-2 was up-regulated while the level of pro-apoptotic protein Bax was down-regulated. Taken together, our results indicate that magnolol induces apoptosis by activation of both mitochondrial and death receptor pathways in A375-S2 cells.Qingjun You, Mingqiu Li, Guoqing Jiao
1956 related Products with: Magnolol induces apoptosis via activation of both mitochondrial and death receptor pathways in A375-S2 cells.
100 ug/vial100ug Lyophilized100ug1x10e7 cells200ul2 Pieces/Box100ug100ug100 μg100 ug100ug Lyophilized
Related Pathways
#15215653 //
To Up
Dracorhodin perchlorate induces apoptosis via activation of caspases and generation of reactive oxygen species.
Dracorhodin perchlorate inhibited proliferation of several tumor cell lines. The drug induced oligonucleosomal fragmentation of DNA in HeLa cells and increased caspase-3, -8, -9 activities followed by the degradation of caspase-3 substrates, inhibitor of caspase-dependent DNase, and poly-(ADP-ribose) polymerase. It also increased caspase-1 activity and a caspase-1 inhibitor, Ac-YVAD-cmk, and a caspase-10 inhibitor z-AEVD-fmk, also reduced dracorhodin-perchlorate-induced HeLa cell death. Dracorhodin perchlorate decreased the expression of anti-apoptotic mitochondrial protein, Bcl-X(L), but not Bcl-2; and it increased the expression of pro-apoptotic protein, Bax. Dracorhodin perchlorate induced a sustained generation of reactive oxygen species (ROS) in HeLa cells; caspase-1 inhibitor, Ac-YVAD-cmk, and caspase-3 inhibitor, z-DEVD-fmk, attenuated the generation of ROS. Taken together, our results indicate that dracorhodin perchlorate alters the intracellular redox status, changed the balance of Bcl-X(L) and Bax protein expression, and induces apoptosis through caspase pathways in HeLa cells.Mingyu Xia, Dong Wang, Minwei Wang, Shin-Ichi Tashiro, Satoshi Onodera, Mutsuhiko Minami, Takashi Ikejima