| Name | NFkappaB (protein family or complex) |
|---|---|
| Synonyms | NF kappa B; NFKB; NFkappaB; Nuclear factor NF kappa B |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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. Normalizing levels of mitochondrial reactive species with each of these agents prevents -induced activation of protein kinase C, formation of advanced glycation end-products, accumulation and NFkappaB activation. |
1(0,0,0,1) | Details |
| 19879948 | Berg EL, Yang J, Melrose J, Nguyen D, Privat S, Rosler E, Kunkel EJ, Ekins S: Chemical target and pathway toxicity mechanisms defined in primary human cell systems. J Pharmacol Toxicol Methods. 2010 Jan-Feb;61(1):3-15. Epub 2009 Oct 29. DISCUSSION: Compounds with diverse mechanisms, including modulators of the NFkappaB pathway, microtubule function and mitochondrial activity, could be discriminated and classified into target and pathway mechanisms in both assay formats. Certain inhibitors of mitochondrial function, such as rotenone and azide, but not others, were classified with inducers of endoplasmic reticulum stress, providing insight into the toxicity mechanisms of these agents. |
1(0,0,0,1) | Details |
| 11764986 | Driscoll KE, Howard BW, Carter JM, Janssen YM, Mossman BT, Isfort RJ: Mitochondrial-derived oxidants and quartz activation of chemokine gene expression. Adv Exp Med Biol. 2001;500:489-96. Rotenone treatment of RLE-6TN cells attenuated peroxide production, NFkappaB activation and MIP-2 gene expression induced by quartz indicating that mitochondria-derived oxidants were contributing to these responses. |
84(1,1,1,4) | Details |
| 17568818 | Geeraerts B, Vanhoecke B, Vanden Berghe W, Philippe J, Offner F, Deforce D: Deguelin inhibits expression of IkappaBalpha protein and induces apoptosis of B-CLL cells in vitro. Leukemia. 2007 Aug;21(8):1610-8. Epub 2007 Jun 14. Deguelin was found to reduce IkappaBalpha protein expression, and thus interacts with the NFkappaB pathway. |
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. TNF-alpha increased nuclear factor (NF)-kappa B-DNA binding, an effect blocked by pretreatment with NAC. |
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. In HEK293 cells, proteasome inhibitors could concentration-dependently increase IL-8 promoter and activator protein-1 (AP-1) activities, but inhibited nuclear factor (NF)-kappa B activation induced by cytokines. The stimulating effects on IL-8 promoter and AP-1 were reduced by diphenyleneiodonium, rotenone and antimycin A. |
1(0,0,0,1) | Details |
| 10704144 | Ruetten H, Thiemermann C, Perretti M: Upregulation of ICAM-1 expression on J774.2 macrophages by endotoxin involves activation of NF-kappaB but not protein tyrosine kinase: comparison to induction of iNOS. Mediators Inflamm. 1999;8(2):77-84. The upregulation of ICAM-1 expression on J774.2 macrophages caused by LPS was significantly inhibited by pretreatment of the cells with inhibitors of the activation of the nuclear transcription factor NF-kappaB, such as L-1-tosylamido-2-phenylethylchloromethyl ketone (TPCK), pyrrolidine dithiocarbamate (PDTC), rotenone or calpain inhibitor I, but not by the kinase inhibitors, tyrphostin AG126 or |
0(0,0,0,0) | Details |
| 7963561 | Suzuki YJ, Mizuno M, Packer L: Signal transduction for nuclear factor-kappa B activation. J Immunol. 1994 Dec 1;153(11):5008-15. Reactive species are thought to be messengers for nuclear factor (NF)-kappa B activation because its activation can be abrogated by antioxidants. The mitochondrial inhibitor, rotenone, also inhibited NF-kappa B activation by calyculin A; however, this inhibition was accompanied by a depletion of cellular ATP. |
1(0,0,0,1) | Details |
| 16140881 | Ilan E, Tirosh O, Madar Z: Triacylglycerol-mediated oxidative stress inhibits production in rat isolated hepatocytes. J Nutr. 2005 Sep;135(9):2090-5. These results suggest that TG reduces production by elevating intracellular ROS levels (prolonged oxidative stress), and the downregulation of NOS enzymes may occur at least in part via the NFkappaB pathway. To evaluate whether the increased oxidative stress inhibited NOS synthesis, cells were treated for 48 h with rotenone (a mitochondrial complex 1 inhibitor) or buthionine sulfoximine (a synthesis inhibitor). |
1(0,0,0,1) | 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. Since blocking either NFkappaB activation or oxidase activity is sufficient to prevent iNOS expression, they are separate targets for therapeutic interventions that aim to modulate iNOS expression in sepsis. Unstimulated endothelial cells produced reactive species (ROS) sensitive to inhibition of oxidase (apocynin and DPI), mitochondrial respiration (rotenone) and NOS (L-NAME). |
1(0,0,0,1) | Details |