Powder: -20°C for 3 years | In solvent: -80°C for 1 year
U0126-EtOH (U0126 Ethanol) 是一种非 ATP 竞争性的选择性MEK1和MEK2抑制剂,IC50分别为 72 nM 和 58 nM。U0126-EtOH 可抑制自噬和线粒体自噬。
规格 | 价格/CNY | 货期 | 数量 | |
---|---|---|---|---|
1 mg | ¥ 167 | 现货 | ||
5 mg | ¥ 383 | 现货 | ||
10 mg | ¥ 617 | 现货 | ||
25 mg | ¥ 995 | 现货 | ||
50 mg | ¥ 1,730 | 现货 | ||
100 mg | ¥ 2,860 | 现货 | ||
200 mg | ¥ 4,180 | 现货 | ||
500 mg | ¥ 6,570 | 现货 | ||
1 mL * 10 mM (in DMSO) | ¥ 417 | 现货 |
产品描述 | U0126-EtOH (U0126 Ethanol) is a non-ATP competitive specific inhibitor of MEK1/2 (IC50: 0.07/0.06 μM). |
靶点活性 | MEK2:60 nM (cell free), MEK1:70 nM (cell free) |
体外活性 | U0126 antagonized AP-1 transcriptional activity via noncompetitive inhibition of the dual specificity kinase MEK with an IC50 of 0.07 microM for MEK 1 and 0.06 microM for MEK 2 [1]. In fibroblasts treated with TPA/serum, U0126 suppressed the up-regulation of c-Fos and c-Jun proteins by 50–80%. Treatment with 10 μM U0126 did not affect the protein levels of the constitutively expressed transcription factors SP-1 or JunD and Fra-1 [2]. U0126 caused phosphorylation and activation of AMPK) and increased phosphorylation of its downstream target acetyl-CoA carboxylase, in HEK293 cells. This effect only occurred in cells expressing the upstream kinase, LKB1 [3]. |
体内活性 | Treatment of mice with U0126 via the aerosol route led to (i) inhibition of MEK activation in the lung (ii) reduction of progeny IAV titers compared to untreated controls (iii) protection of IAV infected mice against a 100× lethal viral challenge [4]. In all U0126 (10.5 mg/kg) experiments, engraftment and early tumor growth were significantly decreased. Furthermore, a 60–70% reduction in the volume of tumors treated with U0126 was obtained 9 days after injection and thereafter. Cdk1 expression was also strongly reduced in U0126-treated mice [5]. |
激酶实验 | The amount of immunoprecipitated wild type MEK used in these assays was adjusted to give a similar amount of activity units as obtained with 10 nM recombinant MEK. All other assays were performed with a recombinant, constitutively activated mutant MEK-1 (ΔN3-S218E/S222D) or constitutively active MEK-2(S222E/S226D). Reaction velocities were measured using a 96-well nitrocellulose filter apparatus as described below. Unless otherwise noted, reactions were carried out at an enzyme concentration of 10 nM, in 20 mM Hepes, 10 mM MgCl2, 5 mM β-mercaptoethanol, 0.1 mg/ml BSA, pH 7.4, at room temperature. Reactions were initiated by the addition of [γ-33P]ATP into the premixed MEK/ERK/inhibitor reaction mixture, and an aliquot of 100 μl was taken every 6 min and transferred to the 96-well nitrocellulose membrane plate which had 50 mM EDTA to stop the reaction. The membrane plate was drawn and washed 4 times with buffer under vacuum. Wells were then filled with 30 μl of Microscint-20 scintillation fluid, and the radioactivity of33P-phosphorylated ERK was counted with a Top Count scintillation counter. Velocities were obtained from the slopes of radioactivity versus time plots. Concentrations of ERK and ATP were 400 nM and 40 μM, respectively, unless otherwise indicated [2]. |
细胞实验 | HEK293 cells were maintained in Dulbecco's modification of Eagle's medium (low glucose) plus 10% foetal bovine serum. HeLa cells stably expressing wild type or kinase-dead LKB1 have been described. AMPK activity was determined by immunoprecipitate kinase assays using anti-AMPK-a1 and -a2 antibodies. Antibodies recognising AMPK phosphorylated on Thr-172 (anti-pT172), AMPK-α1 and -α2 and acetyl-CoA carboxylase-1 (ACC1) phosphorylated on Ser-80 [16] were described previously. Quantification of ratios of signals from phosphorylated and total protein using these antibodies was performed by dual labelling using the LI-COR Odyssey IR imager as described. Contents of ATP and ADP were determined for cells in 6 cm culture dishes by quickly pouring off the medium, adding 350 μl of ice-cold 5% perchloric acid, scraping the cells off with a plastic scraper, and centrifuging (14 000 · g; 3 min, 4 °C) to remove insoluble material. The perchloric acid was then extracted from the supernatant and nucleotides analysed by capillary electrophoresis of perchloric acid extracts as described previously. All incubations of cells were performed in triplicate and results are expressed as means ± S.E.M [3]. |
动物实验 | Prior to injection, FI cells were labeled with a stable fluorescent dye molecule, DiA at 10 μg/ml for 5 h at 37 1C. After washing to remove free DiA, cells were trypsinized for inoculation (U0126 experiments) or transfection (RNAi experiments). Biliary epithelial cells were injected subcutaneously, at the indicated times, into the tibia of nude mice. In the chemical experiments, 3h after inoculation, mice were treated with U0126 (10.5 mg/kg) daily by intraperitoneal injection. The length and width of each tumor were measured every day by using a caliper. The following formula was used to calculate tumor volumes ? width2 length/2. Mice were killed at the end of experiment. Tumors were immediately frozen in liquid nitrogen [5]. |
别名 | U0126 Ethanol, U0126 |
分子量 | 426.6 |
分子式 | C18H16N6S2·C2H6O |
CAS No. | 1173097-76-1 |
Powder: -20°C for 3 years | In solvent: -80°C for 1 year
Ethanol: < 1 mg/mL (insoluble or slightly soluble)
DMSO: 55 mg/mL (128.93 mM)
可选溶剂 | 浓度 体积 质量 | 1 mg | 5 mg | 10 mg | 25 mg |
DMSO | 1 mM | 2.3441 mL | 11.7206 mL | 23.4412 mL | 58.6029 mL |
5 mM | 0.4688 mL | 2.3441 mL | 4.6882 mL | 11.7206 mL | |
10 mM | 0.2344 mL | 1.1721 mL | 2.3441 mL | 5.8603 mL | |
20 mM | 0.1172 mL | 0.586 mL | 1.1721 mL | 2.9301 mL | |
50 mM | 0.0469 mL | 0.2344 mL | 0.4688 mL | 1.1721 mL | |
100 mM | 0.0234 mL | 0.1172 mL | 0.2344 mL | 0.586 mL |
对于不同动物的给药剂量换算,您也可以参考 更多...
请在以下方框中输入您的动物实验信息后点击计算,可以得到母液配置方法和体内配方的制备方法: 比如您的给药剂量是10 mg/kg,每只动物体重20 g,给药体积100 μL,一共给药动物10 只,您使用的配方为5% DMSO+30% PEG300+5% Tween 80+60% ddH2O。那么您的工作液浓度为2 mg/mL。
母液配置方法:2 mg 药物溶于 50 μL DMSO (母液浓度为 40 mg/mL), 如您需要配置的浓度超过该产品的溶解度,请先与我们联系。
体内配方的制备方法:取 50 μL DMSO 主液,加入 300 μL PEG300, 混匀澄清,再加 50 μL Tween 80,混匀澄清,再加 600 μL ddH2O, 混匀澄清。
您可能有的问题的答案可以在抑制剂处理说明中找到,包括如何准备库存溶液,如何存储产品,以及基于细胞的分析和动物实验需要特别注意的问题。
U0126-EtOH 1173097-76-1 Autophagy MAPK Microbiology/Virology Mitophagy Influenza Virus MEK Mitogen-activated protein kinase kinase MAP2K U-0126-EtOH inhibit competitive virus U0126 Ethanol U0126EtOH MAPKK Mitochondrial Autophagy U 0126 Inhibitor progeny non-ATP U0126 EtOH U-0126 U0126 inhibitor