Catalog No.S8276 Synonyms: Trifluoromethoxy carbonylcyanide phenylhydrazone
Molecular Weight(MW): 254.17
FCCP is a potent uncoupler of oxidative phosphorylation in mitochondria that disrupts ATP synthesis by transporting protons across cell membranes.
Cited by 14 Publications
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The changes in 10-N-nonylacridineorange (NAO) fluorescence indicated the cardiolipin (CL) oxidation. In normal cells, NAO could interact with nonoxidized cardiolipin and produces a characteristic green fluorescence. However, after cardiolipin is oxidized, NAO cannot bind to it. F-H, The changes in MDA, GSH, and SOD levels. I and J, The cytoplasmic [Ca2+] map via confocal microscopy by Fluo-2. Fluorescence intensity of Fluo-2 was measured by excitation wavelengths of 340 nm and emission wavelengths of 500 nm. Data (F/F0) were obtained by dividing fluorescence intensity (F) by (F0) at the resting level (t = 0), which was normalized to normal groups. Data are shown as means ± SEM. *P < .05 vs normal group; #P < .05 vs PA group, @P < .05 vs PA + siRNA-NR4A1 or PA + melatonin groups
J Pineal Res, 2018, 64:e12450. FCCP purchased from Selleck.
The mitophagy activity was examined via the overlap of mitochondria and lysosome. Compared to the control cells, Yap-deleted HepG2 cells had more lysosome containing mitochondria. 3-MA was the inhibitor of mitophagy and 3-MA could alleviate the promotive effect of Yap deficiency on mitophagy. FCCP was the inducer of mitophagy, which was used as the positive control group.
Redox Biology, 2018, 14:59-71. FCCP purchased from Selleck.
The mitochondrial fission was observed via immunofluorescence. More shorter mitochondria appeared in response to LPS treatment. However, melatonin treatment could reverse the mitochondrial length. Mdivi1 and FCCP were the inhibitor and activator of mitochondrial fission, respectively.
Cell Stress and Chaperones, 2018, 23(2):281-293. FCCP purchased from Selleck.
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|Description||FCCP is a potent uncoupler of oxidative phosphorylation in mitochondria that disrupts ATP synthesis by transporting protons across cell membranes.|
FCCP treatment induces a very rapid 2-fold increase in intracellular Ca2+ concentration that is accompanied by a strong protein synthesis rate inhibition. The translation inhibition correlates with an increased phosphorylation of the α subunit of eIF2 (eIF2α) and a 1.7-fold increase in the double-stranded RNA-dependent protein kinase activity. FCCP treatment also mildly decreases ATP and reactive oxygen species levels. It increases the expression of mitochondrial genes such as Tfam and COXIV while inducing morphological features of quiescent mouse HSCs and abrogating TGF-β signal transduction.
|In vivo||FCCP significantly reduces mitochondrial membrane potential and ATP production in 8-cell mouse embryos and the number of inner cell mass cells within blastocysts with unchanged blastocyst development. This perturbed embryonic mitochondrial function is concomitant with reduced birth weight in female offspring following embryo transfer, which persists until weaning. Although FCCP-treated males also exhibits reduced glucose tolerance as female, but their insulin sensitivity and adiposity gain between 4 and 14 weeks is unchanged. Reducing mitochondrial function and, thus, decreasing ATP output in the precompacting embryo can influence offspring phenotype.|
|In vitro||DMSO||50 mg/mL (196.71 mM)|
|Ethanol||50 mg/mL (196.71 mM)|
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
|Synonyms||Trifluoromethoxy carbonylcyanide phenylhydrazone|
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