Liproxstatin-1 has been used as a cell death inhibitor in the cell viability assay and for the determination of lipid peroxidation.[1]
Biochem./physiol. Wirkung
Liproxstatin-1 is a potent inhibitor of ferroptosis, a non-apoptotic form of cell death characterized by iron-dependent accumulation of lethal lipid reactive oxygen species (ROS). Liproxstatin-1 suppressed ferroptosis in human cells and in an ischaemia/reperfusion-induced tissue injury model in mice. Knockout of glutathione peroxidase 4 (Gpx4) Has been shown to cause cell death by ferroptosis. Liproxstatin-1 was able to suppress ferroptosis in Gpx4 knock-out mice.
Liproxstatin-1 is a potent inhibitor of ferroptosis.
Ferroptosis is a form of regulated cell death that is driven by lethal accumulation of lipid peroxides upon inhibition of glutathione peroxidase 4 (GPx4). Deletion of the Gpx4 gene in mice revealed that neurons are sensitive to ferroptosis in vivo. However
Ferroptosis-an iron-dependent, non-apoptotic cell death process-is involved in various degenerative diseases and represents a targetable susceptibility in certain cancers1. The ferroptosis-susceptible cell state can either pre-exist in cells that arise from certain lineages or be acquired during cell-state transitions2-5. However
Molecular cancer research : MCR, 18(1), 79-90 (2019-10-24)
Ovarian cancer is the deadliest gynecologic cancer. Despite recent advances, clinical outcomes remain poor, necessitating novel therapeutic approaches. To investigate metabolic susceptibility, we performed nutrigenetic screens on a panel of clear cell and serous ovarian cancer cells and identified cystine
The roles and regulatory mechanisms of ferroptosis (a non-apoptotic form of cell death) in cancer remain unclear. The tumour suppressor BRCA1-associated protein 1 (BAP1) encodes a nuclear deubiquitinating enzyme to reduce histone 2A ubiquitination (H2Aub) on chromatin. Here, integrated transcriptomic
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