|Anisomycin Catalog No.GC11559|
Sample solution is provided at 25 µL, 10mM.
PC-12 cells are seeded in 96-well plates at a concentration of 1×104 cells/well and cultured in an incubator at 37°C with 5% CO2 for at least 12 h prior to exposure to different concentrations of SP600125 (0-80 μM) or Anisomycin (0-20 μM) for 24 h. Subsequently, the culture medium is added to 20 μL of 5 mg/mL MTT working solution and the plate is incubated for 2 h at 37°C. The culture supernatant is removed and the formazan crystals are dissolved in 150 μL DMSO. Finally, the absorbance of each well is measured at 490 nm by a microplate reader. Cell viability is expressed as the percentage of the control group, which is set to 100%.
MiceAdult male TNFRp55/p75 mice, adult male wild-type C57/BL and homozygous Nox2-/- mice are used in this study. Mice are randomized into six experimental groups that undergo the following treatments,. Animals are divided into six groups: group 1: control ischemia/reperfusion, wild-type mice are injected with DMSO (0.1 mL); group 2: Anisomycin+wild-type mice, wild-type mice are injected with Anisomycin (0.1 mg/kg ip); group 3: Anisomycin+TNFR p55/p75-/- mice, TNFR p55/75-/- mice are injected with Anisomycin (0.1 mg/kg ip); group 4: TNFR p55/p75-/- mice, TNFR p55/75-/- mice are not injected with Anisomycin; group 5: Anisomycin+Nox2-/- mice, Nox2-/- mice are injected with Anisomycin (0.1 mg/kg ip); and group 6: Nox2-/- mice, Nox2-/- mice are not injected with Anisomycin. Later (24 h), the hearts are subjected to 30 min of ischemia followed by 30 min of reperfusion.
. Lu Z, et al. Colistin-induced autophagy and apoptosis involves the JNK-Bcl2-Bax signaling pathway and JNK-p53-ROS positive feedback loop in PC-12 cells.
|Chemical Name||(2R,3S,4S)-4-hydroxy-2-(4-methoxybenzyl)pyrrolidin-3-yl acetate|
|Solubility||≥26.5mg/mL in DMSO||Storage||Store at -20°C|
|General tips||For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.|
|Shipping Condition||Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
Anisomycin is a specific agonist of JNK with a concentration of 25 ng/ml .
JNK is short for c-Jun N-terminal kinase which reported as a proapoptotic kinase and plays an important role in many cellular events, such as cell cycle, proliferation, apoptosis and cell stress. It is also reported that JNK plays a pivotal role in the cell apoptosis induced by UV and activated JNK pathway could enhance TNF-α mediated apoptosis thus often regarded as a potent target in clinic  .
Anisomycin is a potent JNK agonist. When tested with hormone refractory cell line DU 145(highly resist to Fas mediated apoptosis), 250 ng/ml anisomysin treatment induced DU145 cells apoptosis together with Fas (200 ng/ml) via activating JNK . In HL-60 cells, treatment of anisomysin activated JNK pathway activity which further induced cell apoptosis . When tested with primary murine embryonic fibroblasts, anisomycin treatment stimulated cell apoptosis via activating JNK expression .
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. Curtin, J.F. and T.G. Cotter, Anisomycin activates JNK and sensitises DU 145 prostate carcinoma cells to Fas mediated apoptosis. Br J Cancer, 2002. 87(10): p. 1188-94.
. Stadheim, T.A. and G.L. Kucera, c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) is required for mitoxantrone- and anisomycin-induced apoptosis in HL-60 cells. Leuk Res, 2002. 26(1): p. 55-65.
. Tournier, C., et al., Requirement of JNK for stress-induced activation of the cytochrome c-mediated death pathway. Science, 2000. 288(5467): p. 870-4.