|1.||Schumacker, Paul T: 3 articles (10/2006 - 06/2002)|
|2.||Marks, Jeremy D: 2 articles (10/2006 - 10/2002)|
|3.||Mack, Mathew M: 2 articles (10/2006 - 10/2002)|
|4.||Waypa, Gregory B: 2 articles (10/2006 - 10/2002)|
|5.||Mungai, Paul T: 2 articles (10/2006 - 10/2002)|
|6.||Kamat, Amrita: 1 article (11/2013)|
|7.||Yeh, Chih-Ko: 1 article (11/2013)|
|8.||Zhang, Hua: 1 article (11/2013)|
|9.||Zhang, Hong-Mei: 1 article (11/2013)|
|10.||Fu, Jian-Liang: 1 article (11/2013)|
12/21/2007 - "Myxothiazol, an inhibitor of mitochondrial electron transfer, did not prevent HIF-1alpha stabilization under moderate hypoxia. "
10/27/2006 - "The mitochondrial inhibitor myxothiazol attenuated the hypoxia-induced changes in the ROS signaling and [Ca(2+)](i), whereas cyanide augmented the increase in [Ca(2+)](i). "
08/15/2002 - "Our data showed that hypoxia increased ROS generation and that hypoxia-induced TLR4 down-regulation was inhibited by myxothiazol, a mitochondrial site III electron transport inhibitor. "
02/01/2011 - "The expression of VEGF in proximal tubular epithelial cells in response to hypoxia was suppressed by the mitochondrial electron transfer inhibitor myxothiazol. "
06/01/2002 - "Brief treatment with exogenous H(2)O(2) during normoxia also induced phosphorylation of p38 as hypoxia, but this effect was not abolished by myxothiazol or DIDS. "
04/01/2005 - "A specific inhibitor of mitochondrial respiration, myxothiazol, caused necrosis of aortae over a similar time course to NO. DETA/NO plus mild hypoxia-induced cell death was substantially reduced by a glycolytic intermediate 3-phosphoglycerate, suggesting that necrosis resulted from energy depletion secondary to respiratory inhibition. "
10/01/2000 - "A 24-h incubation of PC12 cells with NO donors (SNAP or NOC-18) or specific inhibitors of mitochondrial respiration (myxothiazol, rotenone, or azide), in the absence of glucose, caused total ATP depletion and resulted in 80-100% necrosis. "
|3.||Drug-Induced Liver Injury
11/01/2013 - "Human mesangial and teratocarcinoma NT2 cells were used to demonstrate that melatonin-induced oxidation of 2',7'-dichlorodihydrofluorescein (H2 DCF) was inhibited by antimycin A, the MC-3 Qi site-specific inhibitor, but not by myxothiazol, the MC-3 Qo site-specific inhibitor, nor rotenone, the mitochondrial complex I inhibitor. "
|2.||Electron Transport Complex III (Coenzyme Q-Cytochrome-c Reductase)
|8.||Cytochromes b (Cytochrome b)
|9.||Vascular Endothelial Growth Factor A (Vascular Endothelial Growth Factor)
|10.||Vitamin K 3 (Menadione)