BTB06584 inhibits F1Fo-ATPase activity with no effect on ΔΨm or O2 consumption. ATP consumption was decreased following inhibition of respiration, and ischaemic cell death was reduced. BTB06584 efficiency was increased by IF1 overexpression and reduced by silencing the protein. BTB06584 may represent a valuable tool to selectively inhibit mitochondrial F1Fo-ATPase activity without compromising ATP synthesis and to limit ischaemia-induced injury caused by reversal of the mitochondrial F1Fo-ATPsynthase.in vivo: BTB06584 rescues defective haemoglobin synthesis in zebrafish pinotage (pnt) mutants in which expression of the Atpif1a gene is lost.
Kinase Assay
Cell Assay
Animal Administration
References
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