Decylubiquinone | MPTP inhibitor
NMR (Conforms)
Available Options
| Size : | Price | Quantity | |
|---|---|---|---|
| 10 mg | $55.00 | ||
| 50 mg | $220.00 |
Decylubiquinone (55486-00-5) inhibits the Ca2+ dependent mitochondrial permeability transition pore (MPTP) without inhibiting respiration.1 Maximum effect on Ca2+ retention capacity of rat liver mitochondria at 100 μM. Inhibits etoposide-induced apoptosis in in L929 cells at 5 μM via inhibition of cytochrome C release.2 Delays rotenone-induced cardiac dysfunction in a zebrafish model of development and cardiovascular function.3 Substrate for various quinone oxidoreductases.4,5
References/Citations:
1) Fontaine et al. (1998), A Ubiquinone-binding Site Regulates the Mitochondrial Permeability Transition Pore; J. Biol. Chem., 273 25734
2) Karpinich et al. (2002), The course of Etoposide-Induced Apoptosis from Damage to DNA and p53 Activation to Mitochondrial Release of Cytochrome c; J. Biol. Chem., 277 16547
3) Pinho et al. (2013) How mitochondrial dysfunction affects zebrafish development and cardiovascular function: an in vivo model for testing mitochondria-targeted drugs; Br. J. Pharmacol., 169 1072
4) Kunow et al. (1994) F420H2: quinone oxidoreductase from Archaeoglobus fulgidus. Characterization of a membrane-bound multisubunit complex containing FAD and iron-sulfur clusters; Eur. J. Biochem., 223 503
5) Zickermann et al (1998) Analysis of the pathogenic human mitochondria mutation ND1/3460 and mutations of strictly conserved residues in it’s vicinity, using the bacterium Paracoccis denitrificans; Biochemistry, 37 11792
NMR (Conforms)
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Product Data Sheet:
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Decylubiquinone (55486-00-5) inhibits the Ca2+ dependent mitochondrial permeability transition pore (MPTP) without inhibiting respiration.1 Maximum effect on Ca2+ retention capacity of rat liver mitochondria at 100 μM. Inhibits etoposide-induced apoptosis in in L929 cells at 5 μM via inhibition of cytochrome C release.2 Delays rotenone-induced cardiac dysfunction in a zebrafish model of development and cardiovascular function.3 Substrate for various quinone oxidoreductases.4,5
References/Citations:
1) Fontaine et al. (1998), A Ubiquinone-binding Site Regulates the Mitochondrial Permeability Transition Pore; J. Biol. Chem., 273 25734
2) Karpinich et al. (2002), The course of Etoposide-Induced Apoptosis from Damage to DNA and p53 Activation to Mitochondrial Release of Cytochrome c; J. Biol. Chem., 277 16547
3) Pinho et al. (2013) How mitochondrial dysfunction affects zebrafish development and cardiovascular function: an in vivo model for testing mitochondria-targeted drugs; Br. J. Pharmacol., 169 1072
4) Kunow et al. (1994) F420H2: quinone oxidoreductase from Archaeoglobus fulgidus. Characterization of a membrane-bound multisubunit complex containing FAD and iron-sulfur clusters; Eur. J. Biochem., 223 503
5) Zickermann et al (1998) Analysis of the pathogenic human mitochondria mutation ND1/3460 and mutations of strictly conserved residues in it’s vicinity, using the bacterium Paracoccis denitrificans; Biochemistry, 37 11792
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