| Name | protein kinase C (protein family or complex) |
|---|---|
| Synonyms | Protein kinase C; PKC |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 16510472 | Ali MH, Mungai PT, Schumacker PT: Stretch-induced phosphorylation of focal adhesion kinase in endothelial cells: role of mitochondrial oxidants. Am J Physiol Lung Cell Mol Physiol. 2006 Jul;291(1):L38-45. Epub 2006 Mar 1. Strain-induced FAK phosphorylation was abrogated by inhibition of protein kinase C (PKC) with Ro-31-8220 or Go-6976. The mitochondrial inhibitors diphenylene iodonium (5 microM) or rotenone (2 microM) attenuated this increase, whereas L-nitroarginine (100 microM), allopurinol (100 microM), or apocynin (30 microM) had no effect. |
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| 17360324 | Liu Y, Kern JT, Walker JR, Johnson JA, Schultz PG, Luesch H: A genomic screen for activators of the antioxidant response element. Proc Natl Acad Sci U S A. 2007 Mar 20;104(12):5205-10. Epub 2007 Mar 12. Studies with pharmacological inhibitors indicated that 1-phosphatidylinositol 3-kinase and protein kinase C signaling are essential for activity. Overexpression of these cDNAs conferred partial resistance to peroxide or rotenone-induced toxicity, consistent with the induction of antioxidant and phase II detoxification enzymes, which can protect from oxidative stress. |
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| 19429815 | Serpillon S, Floyd BC, Gupte RS, George S, Kozicky M, Neito V, Recchia F, Stanley W, Wolin MS, Gupte SA: production by NAD (P) H oxidase and mitochondria is increased in genetically obese and hyperglycemic rat heart and aorta before the development of cardiac dysfunction. Am J Physiol Heart Circ Physiol. 2009 Jul;297(1):H153-62. Epub 2009 May 8. O (2)(-) levels were elevated (70-90%; P < 0.05) in the diabetic heart, and this elevation was blocked by the Nox inhibitor gp-91 (ds-tat) (50 microM) or by the mitochondrial respiratory chain inhibitors antimycin (10 microM) and rotenone (50 microM). Notably, the activities of Nox and G6PD in the fa/fa rat heart were inhibited by chelerythrine, a protein kinase C inhibitor. |
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| 16737744 | Koutsogiannaki S, Evangelinos N, Koliakos G, Kaloyianni M: Cytotoxic mechanisms of Zn2+ and Cd2+ involve Na+/H+ exchanger (NHE) activation by ROS. Aquat Toxicol. 2006 Jul 20;78(4):315-24. Epub 2006 May 1. The metals effect was reversed after incubation with the amiloride analogue, EIPA, a selective Na+/H+ exchanger (NHE) inhibitor as well as in the presence of calphostin C, a protein kinase C (PKC) inhibitor. Incubation of gill cells with the oxidants rotenone, antimycin A and caused a significant increase in pHi (delta pHi 0.830, 0.272 and 0.610, respectively), while in the presence of the anti-oxidant N-acetyl (NAC) a decrease in pHi (delta pHi -0.090) was measured, indicating that change in reactive species (ROS) production by heavy metals affects NHE activity. |
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| 9777020 | Kuwahara S, Chin S, Delamere NA: Partial inhibition of Na,K-ATPase activity in cultured rabbit non-pigmented ciliary epithelium following an episode of cytoplasmic ATP depletion. Acta Physiol Scand. 1998 Sep;164(1):13-20. Diminished Na,K-ATPase activity was observed in cells that had been pre-treated 10 min with the protein kinase C activator, PDBu, as well as in cells that had been cooled to 4 degrees C for 4 h then rewarmed to 37 degrees C for 30 min (cool-rewarm manoeuvre). In keeping with this suggestion, diminished Na,K-ATPase activity was observed in cells that had been pre-treated 20 min with the metabolic inhibitors CCCP or rotenone and in cells pre-treated 2.5 h in -free medium. |
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| 10079182 | Boldyrev AA, Carpenter DO, Huentelman MJ, Peters CM, Johnson P: Sources of reactive species production in excitotoxin- stimulated cerebellar granule cells. Biochem Biophys Res Commun. 1999 Mar 16;256(2):320-4. Reactive species (ROS) production in rat cerebellar granule cells in the presence of the excitotoxins and kainic acid (KA) and by the protein kinase C activator phorbol (PMA) was Ca2+-dependent and resulted in decreased cell viability. Exposure of stimulated cells to rotenone (a respiratory chain inhibitor) did not decrease ROS levels and did not affect short-term cell viability. |
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| 11961005 | Morigi M, Macconi D, Zoja C, Donadelli R, Buelli S, Zanchi C, Ghilardi M, Remuzzi G: Protein overload-induced NF-kappaB activation in proximal tubular cells requires H (2) O (2) through a PKC-dependent pathway. J Am Soc Nephrol. 2002 May;13(5):1179-89. Specific inhibitors of protein kinase C (PKC) activity significantly prevented H (2) O (2) production and consequent NF-kappaB activation, suggesting that ROS generation in HK-2 cells occurs downstream of PKC activation. To identify the enzymatic sources responsible for the increased H (2) O (2) production, the effect of dyphenyleneiodonium, an inhibitor of the membrane (H) oxidase, was studied, as was the effect of rotenone, which blocks complex I of the mitochondrial respiratory chain. |
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| 15086456 | Lee HB, Yu MR, Song JS, Ha H: Reactive species amplify protein kinase C signaling in high -induced fibronectin expression by human peritoneal mesothelial cells. Kidney Int. 2004 Apr;65(4):1170-9. oxidase inhibitors (diphenyleneiodinium and apocynin) and an inhibitor of mitochondrial electron transport chain subunit I (rotenone) all effectively inhibited high -induced cellular ROS generation and fibronectin secretion. |
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| 11225736 | Li YP, Atkins CM, Sweatt JD, Reid MB: Mitochondria mediate tumor necrosis factor-alpha/NF-kappaB signaling in skeletal muscle myotubes. Antioxid Redox Signal. 1999 Spring;1(1):97-104. We found that activation of NF-kappaB by TNF-alpha was blocked by rotenone or amytal, inhibitors of complex I of the mitochondrial respiratory chain. In addition, we found that TNF-alpha stimulated protein kinase C (PKC) activity. |
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| 18619942 | Wang G, Zeng J, Shen CY, Wang ZQ, Chen SD: Overexpression of Kir2.3 in PC12 cells resists rotenone-induced neurotoxicity associated with PKC signaling pathway. Biochem Biophys Res Commun. 2008 Sep 19;374(2):204-9. Epub 2008 Jul 11. The protection of Kir2.3 against neurodegeneration may be associated with the protein kinase C (PKC) pathway, as PKC is downregulated by Kir2.3 overexpression and the PKC activator can reduce the protective effect of Kir2.3. |
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| 17885094 | Canas N, Valero T, Villarroya M, Montell E, Verges J, Garcia AG, Lopez MG: protects SH-SY5Y cells from oxidative stress by inducing heme oxygenase-1 via phosphatidylinositol 3-kinase/Akt. J Pharmacol Exp Ther. 2007 Dec;323(3):946-53. Epub 2007 Sep 20. Taken together, these results show that CS can protect SH-SY5Y cells under oxidative stress conditions by activating protein kinase C, which phosphorylates Akt that, via the phosphatidylinositol 3-kinase/Akt pathway, induces the synthesis of the antioxidant protein heme oxygenase-1. Cell death caused by a combination of 10 microM rotenone plus 1 microM oligomycin-A (Rot/oligo) was also reduced by CS at concentrations ranging from 0.3 to 100 microM; in this toxicity model, maximum protection was achieved at 3 microM (48%). |
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| 16207877 | Abramov AY, Jacobson J, Wientjes F, Hothersall J, Canevari L, Duchen MR: Expression and modulation of an oxidase in mammalian astrocytes. . J Neurosci. 2005 Oct 5;25(40):9176-84. This was independent of mitochondrial ROS production, because it was unaffected by mitochondrial depolarization with rotenone and oligomycin. |
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| 15567152 | Tsubouchi H, Inoguchi T, Inuo M, Kakimoto M, Sonta T, Sonoda N, Sasaki S, Kobayashi K, Sumimoto H, Nawata H: Sulfonylurea as well as elevated levels stimulate reactive species production in the pancreatic beta-cell line, MIN6-a role of NAD (P) H oxidase in beta-cells. Biochem Biophys Res Commun. 2005 Jan 7;326(1):60-5. This effect was completely blocked by NAD (P) H oxidase inhibitor (diphenylene iodonium) and protein kinase C (PKC) inhibitor (calphostin C), but not affected by other flavoprotein inhibitors (rotenone, or l-N-monomethyl |
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| 16895947 | Aitken RJ, Wingate JK, De Iuliis GN, Koppers AJ, McLaughlin EA: Cis-unsaturated fatty acids stimulate reactive species generation and lipid peroxidation in human spermatozoa. J Clin Endocrinol Metab. 2006 Oct;91(10):4154-63. Epub 2006 Aug 8. This effect could not be blocked with inhibitors of the cyclooxygenase or lipoxygenase pathways of AA metabolism, rotenone, protein kinase C antagonists, or known inhibitors of plasma membrane redox systems. |
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| 10783895 | Nishikawa T, Edelstein D, Du XL, Yamagishi S, Matsumura T, Kaneda Y, Yorek MA, Beebe D, Oates PJ, Hammes HP, Giardino I, Brownlee M: Normalizing mitochondrial production blocks three pathways of hyperglycaemic damage. Nature. 2000 Apr 13;404(6779):787-90. Three seemingly independent biochemical pathways are involved in the pathogenesis: -induced activation of protein kinase C isoforms; increased formation of -derived advanced glycation end-products; and increased flux through the aldose reductase pathway. |
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| 19576886 | Matsuo J, Oku H, Kanbara Y, Kobayashi T, Sugiyama T, Ikeda T: Involvement of oxidase and protein kinase C in endothelin-1-induced production in retinal microvessels. Exp Eye Res. 2009 Nov;89(5):693-9. Epub 2009 Jul 2. In addition, the changes induced by adding apocynin (10 microM), myr-PKC (1.0 microM), allopurinol (100 microM), rotenone (10 microM), or L-NAME (100 microM) with ET-1 were evaluated. |
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| 9893134 | Heitzer T, Wenzel U, Hink U, Krollner D, Skatchkov M, Stahl RA, MacHarzina R, Brasen JH, Meinertz T, Munzel T: Increased NAD (P) H oxidase-mediated production in renovascular hypertension: evidence for an involvement of protein kinase C. Kidney Int. 1999 Jan;55(1):252-60. Vascular O-.2 was normalized by the PKC inhibitor calphostin C, by the inhibitor of flavin-dependent oxidases, diphenylene iodonium, and recombinant -binding superoxide dismutase, whereas inhibitors of the xanthine oxidase synthase (NG-nitro- and mitochondrial NADH dehydrogenase (rotenone) were ineffective. |
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| 12821678 | Hua H, Munk S, Goldberg H, Fantus IG, Whiteside CI: High glucose-suppressed endothelin-1 Ca2+ signaling via oxidase and diacylglycerol-sensitive protein kinase C isozymes in mesangial cells. J Biol Chem. 2003 Sep 5;278(36):33951-62. Epub 2003 Jun 23. Pretreatment with carbonyl m-chlorophenylhydrazone or rotenone did not restore Ca2+ signaling in HG. |
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| 9200650 | Alcazar O, Qiu-yue Z, Gine E, Tamarit-Rodriguez J: Stimulation of islet protein kinase C translocation by requires metabolism of the fatty acid. Diabetes. 1997 Jul;46(7):1153-8. |
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| 17540012 | Egea J, Rosa AO, Cuadrado A, Garcia AG, Lopez MG: Nicotinic receptor activation by epibatidine induces heme oxygenase-1 and protects chromaffin cells against oxidative stress. J Neurochem. 2007 Sep;102(6):1842-52. Epub 2007 Jun 1. In this context, we investigated here if the exposure of bovine chromaffin cells to the potent nAChR agonist epibatidine protected against rotenone (30 micromol/L) plus oligomycin (10 micromol/L) (rot/oligo) toxicity, an in vitro model of mitochondrial ROS production. Pre-incubation with dantrolene (100 micromol/L) (a blocker of the ryanodine receptor channel), chelerythrine (1 micromol/L) (a protein kinase C inhibitor), or PD98059 (50 micromol/L) (a MEK inhibitor), aborted epibatidine-elicited cytoprotection. |
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| 9780311 | Aten RF, Kolodecik TR, Rossi MJ, Debusscher C, Behrman HR: treatment in vivo, but not in vitro, stimulates protein kinase C-activated production by nonsteroidogenic cells of the rat corpus luteum. Biol Reprod. 1998 Nov;59(5):1069-76. In conclusion, there is a generator in luteinized ovaries that is activated through a protein kinase C pathway, localized in nonsteroidogenic cells, transiently increased during PGF2alpha-induced luteolysis in vivo, and elevated during natural luteal regression. The response to TPA and zymosan was inhibited by the /-oxidase inhibitor, diphenylene iodonium (ID50 = 5 microM for TPA), but not by the mitochondrial inhibitors, rotenone, or azide. |
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| 7529030 | Zulueta JJ, Yu FS, Hertig IA, Thannickal VJ, Hassoun PM: Release of peroxide in response to hypoxia-reoxygenation: role of an NAD (P) H oxidase-like enzyme in endothelial cell plasma membrane. Am J Respir Cell Mol Biol. 1995 Jan;12(1):41-9. Furthermore, inhibitors of cyclooxygenase (indomethacin), phospholipase A2 (quinacrine and chlorpromazine), synthase analogs), the mitochondrial electron transport chain (rotenone and and cytochrome P-450 (methoxypsoralen) had no or minimal effect on this release. On the other hand, inhibitors of protein kinase C (calphostin and staurosporine) and oxidase (diphenyliodonium) reduced the release of H2O2 from EC in a dose-dependent manner in both exposure groups. |
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| 15133064 | Cuchillo-Ibanez I, Lejen T, Albillos A, Rose SD, Olivares R, Villarroya M, Garcia AG, Trifaro JM: Mitochondrial sequestration and protein kinase C cooperate in the regulation of cortical F-actin disassembly and secretion in bovine chromaffin cells. J Physiol. 2004 Oct 1;560(Pt 1):63-76. Epub 2004 May 7. In addition, rotenone and oligomycin A, two other mitochondrial inhibitors, also evoked cortical F-actin disassembly and potentiated secretion; again, these effects were blocked by chelerythrine. |
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| 7599232 | Hoek JB, Farber JL, Thomas AP, Wang X: -dependent signalling and mitochondrial dysfunction: mitochondrial uptake during hormonal stimulation in intact liver cells and its implication for the mitochondrial permeability transition. Biochim Biophys Acta. 1995 May 24;1271(1):93-102. This effect of was mimicked by phorbol ester, suggesting a role for protein kinase C. Mitochondrial Ca2+ accumulation was determined by following the ionomycin-induced Ca2+ release in permeabilized cells and mitochondrial swelling was studied by following cyclosporin A-sensitive light scattering changes induced by phenyl-arsenoxide and rotenone. |
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