Ferroptosis

The oncogenic RAS-selective lethal small molecule erastin triggers a unique iron-dependent form of non-apoptotic cell death termed ferroptosis. Ferroptotic death is morphologically, biochemically and genetically distinct from apoptosis, various forms of necrosis, and autophagy. This process is characterized by the overwhelming, iron-dependent accumulation of lethal lipid ROS. Unlike other forms of apoptotic and non-apoptotic death, this requirement for ROS accumulation appears to be universal.
The specific role of iron in ferroptosis is yet unclear. Ferroptosis cannot be explained by a simple increase in H2O2-dependent, iron-catalyzed ROS production (i.e. Fenton chemistry), as H2O2-induced death is distinct from RSL-induced ferroptosis[1]. Glutathione (GSH) peroxidase 4 (GPX4) is a crucial inhibitor of ferroptosis, and its activity relies on GSH levels. Despite a clear mechanistic overlap between oxytosis and ferroptosis, including the dependence on inhibition of the system Xc Cys/Glu antiporter, a decrease in GSH levels and the presence of lipid peroxidation, ferroptosis seems to depend mainly on iron instead of calcium signaling[2].

KEYWORDS: Ferroptosis | inhibitor | supplier | oncogenic |RAS| lethal | erastiniron-dependent | non-apoptotic | apoptosis | necrosis | autophagy | accumulation | lipidROS| Glutathione |GSH| peroxidase 4 |GPX4


[1] S.J. Dixon et al. Ferroptosis: an iron-dependent form of nonapoptotic cell death. Cell. 2012, 149, 1060-1072.
[2] T. Vanden Berghe et al. Regulated necrosis: the expanding network of non-apoptotic cell death pathways. Nat. Rev. Mol. Cell Biol. 2014, 15, 135-147. 

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2293 Ferrostatin 1 Potent inhibitor of erastin-induced ferroptosis €85.00

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