S
Satoshi Onodera
Researcher at Showa Pharmaceutical University
Publications - 171
Citations - 5629
Satoshi Onodera is an academic researcher from Showa Pharmaceutical University. The author has contributed to research in topics: Apoptosis & Autophagy. The author has an hindex of 42, co-authored 171 publications receiving 5073 citations.
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Autophagy preceded apoptosis in oridonin-treated human breast cancer MCF-7 cells.
TL;DR: Oridonin simultaneously induced MCF-7 cells both apoptosis and autophagy, and in this settings, inhibition of Autophagy induced lowered apoptotic level, therefore,Autophagy participated in upregulation of apoptosis.
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ERK and JNK mediate TNFα-induced p53 activation in apoptotic and autophagic L929 cell death
TL;DR: It is demonstrated that TNFalpha-induced MAPKs mediate p53 activation in apoptotic and autophagic cell death, as well as autophagy may amplify apoptosis when associated with a death signaling pathway.
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Reactive Oxygen Species Mediate Oridonin-Induced HepG2 Apoptosis Through p53, MAPK, and Mitochondrial Signaling Pathways
TL;DR: This study showed that oridonin stimulated mitochondrial transmembrane permeabilization in a ROS-dependent manner because NAC almost thoroughly reversed the drop of mitochondrial trans Membrane potential (Deltapsim) and the release of cytochrome c from the mitochondrial inter-membranes space into cytosol.
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Inhibition of EGFR signaling augments oridonin-induced apoptosis in human laryngeal cancer cells via enhancing oxidative stress coincident with activation of both the intrinsic and extrinsic apoptotic pathways
TL;DR: It is shown that inhibition of EGFR with tyrphostin AG1478 enhances oridonin-induced cell death in human laryngeal cancer cells HEp-2, a cell line characterized by EGFR gene amplification.
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Reactive oxygen species and nitric oxide regulate mitochondria-dependent apoptosis and autophagy in evodiamine-treated human cervix carcinoma HeLa cells.
TL;DR: This study reported that reactive oxygen species and nitric oxide generations were induced by evodiamine time-dependently; while they acted in synergy to trigger mitochondria-dependent apoptosis by induction of mitochondrial membrane permeabilization (MMP) through increasing the Bax/Bcl-2 or Bcl-xL ratio.