Title : zVAD-induced autophagic cell death requires c-Src-dependent ERK and JNK activation and reactive oxygen species generation.

Pub. Date : 2011 Feb

PMID : 21127402






4 Functional Relationships(s)
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1 zVAD also stimulated PARP activation, and the PARP inhibitor DPQ can reduce zVAD-induced cell death, but did not affect ROS production, suggesting the increased ROS leads to PARP activation and cell death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone poly (ADP-ribose) polymerase family, member 1 Mus musculus
2 zVAD also stimulated PARP activation, and the PARP inhibitor DPQ can reduce zVAD-induced cell death, but did not affect ROS production, suggesting the increased ROS leads to PARP activation and cell death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone poly (ADP-ribose) polymerase family, member 1 Mus musculus
3 zVAD also stimulated PARP activation, and the PARP inhibitor DPQ can reduce zVAD-induced cell death, but did not affect ROS production, suggesting the increased ROS leads to PARP activation and cell death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone poly (ADP-ribose) polymerase family, member 1 Mus musculus
4 In conclusion, we confirm the autophagic death in zVAD-treated L929 cells, and define a new molecular pathway in which Src-dependent ERK and JNK activation can link a signal from caspase inhibition to autophagy, which in turn induce ROS production and PARP activation, eventually leading to necroptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone poly (ADP-ribose) polymerase family, member 1 Mus musculus