| Name | p47phox |
|---|---|
| Synonyms | 47 kDa autosomal chronic granulomatous disease protein; 47 kDa neutrophil oxidase factor; NCF 1; NCF 47K; NCF1; NCF1A; NOXO 2; NOXO2… |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 19781192 | Chen Y, Zhang AH, Huang SM, Ding GX, Zhang WZ, Bao HY, Wu HM, Chen RH: oxidase-derived reactive species involved in angiotensin II-induced monocyte chemoattractant protein-1 expression in mesangial cells]. Zhonghua Bing Li Xue Za Zhi. 2009 Jul;38(7):456-61. In contrast, inhibitors of other oxidant-producing enzymes, including the mitochondrial complex Iinhibitor rotenone, the xanthine oxidase inhibitor allopurinol, the cyclooxygenase inhibitor indomethacin, the lipoxygenase inhibitor nordihydroguiaretic acid, the cytochrome P450 oxygenase inhibitor ketoconazole and the synthase inhibitor G-nitro- methyl ester were without an effect. oxidase activity was examined by lucigenin chemiluminescence. p47phox and p67phox translocation was assayed by Western blot. |
2(0,0,0,2) | Details |
| 15328001 | Alba G, El Bekay R, Alvarez-Maqueda M, Chacon P, Vega A, Monteseirin J, Santa Maria C, Pintado E, Bedoya FJ, Bartrons R, Sobrino F: Stimulators of AMP-activated protein kinase inhibit the respiratory burst in human neutrophils. FEBS Lett. 2004 Aug 27;573(1-3):219-25. AMPK activated with either or with 5'-AMP significantly attenuated both phorbol 12- 13- (PMA) and formyl methionyl leucyl -stimulated O2- release by human neutrophils, consistently with a reduced translocation to the cell membrane and phosphorylation of a cytosolic component of oxidase, namely p47phox. |
1(0,0,0,1) | Details |
| 9886268 | Sambo P, Jannino L, Candela M, Salvi A, Donini M, Dusi S, Luchetti MM, Gabrielli A: Monocytes of patients wiht systemic sclerosis (scleroderma spontaneously release in vitro increased amounts of J Invest Dermatol. 1999 Jan;112(1):78-84. The involvement of oxidase in the enhanced 02*- production was demonstrated by the finding that the cytosolic components of the enzyme, p47phox and p67phox, were both translocated to the plasma membrane of enriched but otherwise unmanipulated monocytes of SSc patients. The involvement of mitochondrial oxidases was excluded by the lack of inhibition of O2*- production when monocytes were incubated in the presence of rotenone, a mitochondrial oxidase inhibitor. |
1(0,0,0,1) | Details |
| 15111505 | Ceolotto G, Bevilacqua M, Papparella I, Baritono E, Franco L, Corvaja C, Mazzoni M, Semplicini A, Avogaro A: Insulin generates free radicals by an NAD (P) H, phosphatidylinositol 3'-kinase-dependent mechanism in human skin fibroblasts ex vivo. Diabetes. 2004 May;53(5):1344-51. Furthermore, insulin-induced O (2)(-) production was attenuated by the NAD (P) H inhibitor apocynin, but not by rotenone or The insulin-induced free radical production led to membranous translocation of p47phox and markedly enhanced ERK-1 and -2 activation in human fibroblasts. |
1(0,0,0,1) | Details |
| 16571865 | Li Z, Hyseni X, Carter JD, Soukup JM, Dailey LA, Huang YC: Pollutant particles enhanced H2O2 production from NAD (P) H oxidase and mitochondria in human pulmonary artery endothelial cells. Am J Physiol Cell Physiol. 2006 Aug;291(2):C357-65. Epub 2006 Mar 29. Knockdown of p47phox gene expression by small interfering RNA attenuated UP-induced H2O2 production and phosphorylation of ERK1/2 and p38 MAPKs. Inhibitors of other H2O2-producing enzymes, including Nomega-methyl-L-argnine, indomethacin, allopurinol, cimetidine, rotenone, and antimycin, had no effects. |
1(0,0,0,1) | Details |
| 12615666 | Ungvari Z, Csiszar A, Edwards JG, Kaminski PM, Wolin MS, Kaley G, Koller A: Increased production in coronary arteries in hyperhomocysteinemia: role of tumor necrosis factor-alpha, NAD (P) H oxidase, and inducible synthase. Arterioscler Thromb Vasc Biol. 2003 Mar 1;23(3):418-24. Epub 2003 Feb 13. METHODS AND RESULTS: The increased generation of O2*- by HHcy coronary arteries was inhibited by SOD, diphenyleneiodonium, apocynin, and apocynin plus amino but was unaffected by allopurinol and rotenone. Expression of p67phox, p22phox, and p47phox subunits and that of endothelial nitric oxide synthase, Cu,Zn-SOD, Mn-SOD, extracellular SOD (mRNA), and xanthine oxidase was unchanged. |
1(0,0,0,1) | Details |
| 15544846 | Springer J, Pleimes D, Scholz FR, Fischer A: Substance P mediates AP-1 induction in A549 cells via reactive species. Regul Pept. 2005 Jan 15;124(1-3):99-103. The likely source of ROS are the mitochondria as rotenone inhibited AP-1 induction and the p47phox subunit of the oxidase complex, responsible for ROS generation in phagocytotic cells, was not expressed in A549 cells assayed by RT-PCR. |
0(0,0,0,0) | Details |
| 17320767 | Liu S, Ma X, Gong M, Shi L, Lincoln T, Wang S: down-regulation of -dependent protein kinase I expression in vascular smooth muscle cells involves NAD (P) H oxidase-derived reactive species. Free Radic Biol Med. 2007 Mar 15;42(6):852-63. Epub 2007 Jan 3. High glucose exposure time-dependently increased production in VSMC, which was abolished by tempol or apocynin treatment, but not by other inhibitors of -producing enzymes (L-NAME, rotenone, or Total protein levels and phosphorylated levels of p47phox (an oxidase subunit) were increased in VSMC after high exposure. |
3(0,0,0,3) | Details |
| 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. Likewise, catalase or p47phox antisense oligonucleotide normalized the [Ca2+] i response to ET-1 in HG to 521 +/- 58 nM and 514 +/- 48 nM, respectively. Pretreatment with carbonyl m-chlorophenylhydrazone or rotenone did not restore Ca2+ signaling in HG. |
3(0,0,0,3) | Details |
| 11710721 | Sambo P, Baroni SS, Luchetti M, Paroncini P, Dusi S, Orlandini G, Gabrielli A: Oxidative stress in scleroderma: maintenance of scleroderma fibroblast phenotype by the constitutive up-regulation of reactive species generation through the oxidase complex pathway. Arthritis Rheum. 2001 Nov;44(11):2653-64. This suppression was not seen with rotenone, a mitochondrial oxidase inhibitor, or allopurinol, a xanthine oxidase inhibitor. To verify oxidase activation, the light membrane of fibroblasts was immunoblotted with an anti-p47phox-specific antibody. |
2(0,0,0,2) | Details |
| 18481258 | Wu F, Tyml K, Wilson JX: iNOS expression requires oxidase-dependent redox signaling in microvascular endothelial cells. J Cell Physiol. 2008 Oct;217(1):207-14. Unstimulated endothelial cells produced reactive species (ROS) sensitive to inhibition of oxidase (apocynin and DPI), mitochondrial respiration (rotenone) and NOS (L-NAME). LPS + IFNgamma caused a marked increase in ROS production; this increase was abolished by inhibition of oxidase (apocynin, DPI and p47phox deficiency). |
2(0,0,0,2) | Details |