Protein Information

Name AP 1 (protein family or complex)
Synonyms AP 1; AP 1 complex; AP1; Adapter related protein complex 1

Compound Information

Name rotenone
CAS

Reference List

PubMed Abstract RScore(About this table)
15557194 Woo CH, Lim JH, Kim JH: Lipopolysaccharide induces matrix metalloproteinase-9 expression via a mitochondrial reactive oxygen 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 oxygen 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 N-acetylcysteine, glutathione, diphenyleneiodonium, rotenone and antimycin A.
83(1,1,1,3) Details
15897899 Felty Q, Singh KP, Roy D: Estrogen-induced G1/S transition of G0-arrested estrogen-dependent 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.
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 oxygen 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 NADPH 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 glutathione 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 hydrogen peroxide generation in ceramide-induced apoptosis. J Biol Chem. 1997 Aug 22;272(34):21388-95.

We also present evidence that ceramide-induced activation of the transcription factors NF-kappaB and AP-1 is mediated by mitochondrial derived reactive oxygen 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, N-acetylcysteine and pyrrolidine dithiocarbamate.
1(0,0,0,1) Details