Claim · model-written summary
The proteasome inhibitor MG132 suppressed H2O2-induced PCD in BY-2 cells.
- Taxon
- tobacco Bright Yellow-2 (BY-2) cellse0
- Treatment
- proteasome inhibitor MG132e4
- Outcome
- H2O2-induced PCDe4
- Direction
- suppressede4
Not reportedMaterialGeneCompoundOrgan / stageInteractorInteractor roleSecond interactorSecond interactor roleComparatorSettingValueQualifier
Verbatim
e0“H2O2-induced programmed cell death (PCD) of tobacco Bright Yellow-2 (BY-2) cells”
e4“The proteasome inhibitor MG132 suppressed the H2O2-induced PCD”
Title
Md. Sanaullah Biswas; Ryota Terada; Jun’ichi Mano Antioxidants 2020. doi:10.3390/antiox9020141
Other claims from this paper (7)
- Intervention effect The C3LP activity increased twofold after a lethal dose of H2O2 but not after a sublethal dose in BY-2 cells.
- Intervention effect Intracellular RCS levels (4-hydroxy-(E)-hexenal and HNE) increased 1.2–1.5-fold after a lethal dose of H2O2 in BY-2 cells.
- Intervention effect NADPH-dependent carbonyl reductase activity decreased after a lethal dose of H2O2 in BY-2 cells.
- Mechanism The C3LP activity of the beta1 subunit of the 20S proteasome is responsible for PCD in BY-2 cells.
- Intervention effect H2O2 added to cell-free protein extract inactivated the carbonyl reductase.
- Mechanism The authors propose that H2O2 inactivates a carbonyl reductase, letting RCS rise and activating C3LP activity of the 20S proteasome, which triggers PCD.
- Mechanism The carbonyl reductase acts as an ROS sensor for triggering PCD in BY-2 cells.