Size: | Price | Quantity | |
---|---|---|---|
200 µg | $45.00 | ||
1 mg | $140.00 |
Piericidin A (2738-64-9) is a potent inhibitor of the mitochondrial and bacterial type I NADH-ubiquinone oxidoreductase (complex I).1 Piericidin A is a ubiquinone analog which binds to the ubiquinone binding site of the enzyme.2 It is an extremely useful tool for exploring the role of complex I in mitochondrial function in both normal and pathophysiology.3-5 Prevents upregulation of GRP78 and induces cell death in glucose-deprived, etoposide-resistant HT-29 cells (IC50=7.7 nM).6
References/Citations:
1) Fato et al. (2009), Differential effects of mitochondrial Complex I inhibitors on production of reactive oxygen species; Biochim. Biophys. Acta, 1787 384
2) Zhou and Fenical (2016), The unique chemistry and biology of the piericidins; J. Antibiot. (Tokyo), 69 582
3) Bongard et al. (2015), The effects of mitochondrial complex I blockade on ATP and permeability in rat pulmonary microvascular endothelial cells in culture (PMVEC) are overcome by coenzyme Q1 (CoQ1); Free Radic. Biol. Med., 79 69
4) Lee et al. (2013), Isoniazid-induced cell death is precipitated by underlying mitochondrial complex I dysfunction in mouse hepatocytes; Free Radic. Biol. Med., 65 584
5) Choi et al. (2011), Loss of mitochondrial complex I activity potentiates dopamine neuron death induced by microtubule dysfunction in a parkinson’s disease model; J. Cell Biol., 192 873
6) Hwang et al. (2008), Etoposide-resistant HT-29 human colon carcinoma cells during glucose deprivation are sensitive to piericidin A, a GRP78 down regulator; J. Cell Physiol., 215 243
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Piericidin A (2738-64-9) is a potent inhibitor of the mitochondrial and bacterial type I NADH-ubiquinone oxidoreductase (complex I).1 Piericidin A is a ubiquinone analog which binds to the ubiquinone binding site of the enzyme.2 It is an extremely useful tool for exploring the role of complex I in mitochondrial function in both normal and pathophysiology.3-5 Prevents upregulation of GRP78 and induces cell death in glucose-deprived, etoposide-resistant HT-29 cells (IC50=7.7 nM).6
References/Citations:
1) Fato et al. (2009), Differential effects of mitochondrial Complex I inhibitors on production of reactive oxygen species; Biochim. Biophys. Acta, 1787 384
2) Zhou and Fenical (2016), The unique chemistry and biology of the piericidins; J. Antibiot. (Tokyo), 69 582
3) Bongard et al. (2015), The effects of mitochondrial complex I blockade on ATP and permeability in rat pulmonary microvascular endothelial cells in culture (PMVEC) are overcome by coenzyme Q1 (CoQ1); Free Radic. Biol. Med., 79 69
4) Lee et al. (2013), Isoniazid-induced cell death is precipitated by underlying mitochondrial complex I dysfunction in mouse hepatocytes; Free Radic. Biol. Med., 65 584
5) Choi et al. (2011), Loss of mitochondrial complex I activity potentiates dopamine neuron death induced by microtubule dysfunction in a parkinson’s disease model; J. Cell Biol., 192 873
6) Hwang et al. (2008), Etoposide-resistant HT-29 human colon carcinoma cells during glucose deprivation are sensitive to piericidin A, a GRP78 down regulator; J. Cell Physiol., 215 243
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