Title : Identification of Frataxin as a regulator of ferroptosis.

Pub. Date : 2020 May

PMID : 32169822






7 Functional Relationships(s)
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1 In the present study, we demonstrate that the protein Frataxin (FXN) is a key regulator of ferroptosis by modulating iron homeostasis and mitochondrial function. Iron frataxin Homo sapiens
2 In the present study, we demonstrate that the protein Frataxin (FXN) is a key regulator of ferroptosis by modulating iron homeostasis and mitochondrial function. Iron frataxin Homo sapiens
3 Suppression of FXN expression specifically repressed the proliferation, destroyed mitochondrial morphology, impeded Fe-S cluster assembly and activated iron starvation stress. Iron frataxin Homo sapiens
4 Suppression of FXN expression specifically repressed the proliferation, destroyed mitochondrial morphology, impeded Fe-S cluster assembly and activated iron starvation stress. Iron frataxin Homo sapiens
5 Moreover, suppression of FXN expression significantly enhanced erastin-induced cell death through accelerating free iron accumulation, lipid peroxidation and resulted in dramatic mitochondria morphological damage including enhanced fragmentation and vanished cristae. Iron frataxin Homo sapiens
6 Vice versa, enforced expression of FXN blocked iron starvation response and erastin-induced ferroptosis. Iron frataxin Homo sapiens
7 More importantly, pharmacological or genetic blocking the signal of iron starvation could completely restore the resistance to ferroptosis in FXN knockdown cells and xenograft graft in vivo. Iron frataxin Homo sapiens