Name | AP 1 (protein family or complex) |
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Synonyms | AP 1; AP 1 complex; AP1; Adapter related protein complex 1 |
Name | rotenone |
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CAS |
PubMed | Abstract | RScore(About this table) | |
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15557194 | Woo CH, Lim JH, Kim JH: Lipopolysaccharide induces matrix metalloproteinase-9 expression via a mitochondrial reactive species-p38 kinase-activator protein-1 pathway in Raw 264.7 cells. J Immunol. 2004 Dec 1;173(11):6973-80. LPS-induced MMP-9 expression and p38 kinase phosphorylation were also inhibited by rotenone, a specific inhibitor of mitochondrial complex I, supporting the role of mitochondrial ROS in LPS signaling to MMP-9. Taken together, our findings identify a ROS-p38 kinase-AP-1 cascade as a novel pathway mediating LPS signaling to MMP-9 expression in macrophages. |
1(0,0,0,1) | Details |
12208513 | Wu HM, Chi KH, Lin WW: Proteasome inhibitors stimulate activator protein-1 pathway via reactive species production. FEBS Lett. 2002 Aug 28;526(1-3):101-5. The stimulating effects on IL-8 promoter and AP-1 were reduced by diphenyleneiodonium, rotenone and antimycin A. |
83(1,1,1,3) | Details |
15897899 | Felty Q, Singh KP, Roy D: breast cancer cells is regulated by mitochondrial oxidant signaling. Oncogene. 2005 Jul 21;24(31):4883-93. Furthermore, E2-induced binding of AP-1 and CREB to the TRE and CRE response sequences, respectively, in the promoter of cyclin D1 was inhibited by NAC or rotenone. |
-induced G1/S transition of G0-arrested -dependent 31(0,1,1,1) | 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. |
5(0,0,0,5) | Details |
11382920 | Hoffmann A, Gloe T, Pohl U: Hypoxia-induced upregulation of eNOS gene expression is redox-sensitive: a comparison between hypoxia and inhibitors of cell metabolism. J Cell Physiol. 2001 Jul;188(1):33-44. In order to study a potential role of the redox regulated transcription factor complex AP-1 in hypoxia-induced eNOS mRNA transcription, c-jun expression was determined and decoy experiments were performed. c-jun expression paralleled changes of eNOS mRNA expression and MTT-reduction. Therefore, cultured porcine aortic endothelial cells (PAEC) were exposed to hypoxia (1-10% O (2)) or inhibitors of cellular energy metabolism including rotenone, 2, 4 dinitrophenol (DNP) and 2-deoxyglucose for 6 to 24 h. |
3(0,0,0,3) | Details |
9374527 | Morales A, Garcia-Ruiz C, Miranda M, Mari M, Colell A, Ardite E, Fernandez-Checa JC: Tumor necrosis factor increases hepatocellular by transcriptional regulation of the heavy subunit chain of gamma-glutamylcysteine synthetase. J Biol Chem. 1997 Nov 28;272(48):30371-9. Thus, TNF increases hepatocellular GSH levels by transcriptional regulation of gamma-GCS-HS gene, probably through AP-1/metal response element-like binding site (s) in its promoter, which may constitute a protective mechanism in the control of oxidative stress induced by inflammatory cytokines. |
1(0,0,0,1) | Details |
8760145 | Warner BB, Stuart L, Gebb S, Wispe JR: Redox regulation of manganese superoxide dismutase. . Am J Physiol. 1996 Jul;271(1 Pt 1):L150-8. DNA binding of two redox-sensitive transcription factors, NF-kappa B and activator protein (AP)-1, was evaluated. |
1(0,0,0,1) | Details |
9261153 | Quillet-Mary A, Jaffrezou JP, Mansat V, Bordier C, Naval J, Laurent G: Implication of mitochondrial We also present evidence that -induced activation of the transcription factors NF-kappaB and AP-1 is mediated by mitochondrial derived reactive species. Both H2O2 production, transcription factor activation as well as apoptosis could be inhibited by rotenone and thenoyltrifluoroacetone (specific mitochondrial complexes I and II inhibitors) and antioxidants, and pyrrolidine dithiocarbamate. |
peroxide generation in -induced apoptosis. J Biol Chem. 1997 Aug 22;272(34):21388-95.1(0,0,0,1) | Details |