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Anisomycin Catalog No.GC11559

JNK agonist, potent and specific

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10mM (in 1mL DMSO)
$35.00
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10mg
$36.00
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50mg
$72.00
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500mg
$610.00
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1g
$1,090.00
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Sample solution is provided at 25 µL, 10mM.

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Protocol

Cell experiment:

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%[1].

Animal experiment:

Mice[2]Adult 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[2].

References:

[1]. 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.
[2]. Gao X, et al. Transcriptional regulation of stress kinase JNK2 in pro-arrhythmic CaMKIIδ expression in the aged atrium. Cardiovasc Res. 2018 Apr 1;114(5):737-746.
[3]. Zhao TC, et al. Disruption of Nox2 and TNFRp55/p75 eliminates cardioprotection induced by Anisomycin. Am J Physiol Heart Circ Physiol. 2012 Nov 15;303(10):H1263-72.

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Chemical Properties

Cas No. 22862-76-6 SDF
Synonyms N/A
Chemical Name (2R,3S,4S)-4-hydroxy-2-(4-methoxybenzyl)pyrrolidin-3-yl acetate
Canonical SMILES O[C@@H]1[C@H]([C@@H](CC(C=C2)=CC=C2OC)NC1)OC(C)=O
Formula C14H19NO4 M.Wt 265.31
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

Background

Anisomycin is a specific agonist of JNK with a concentration of 25 ng/ml [1].

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 [2] [3].

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 [4]. In HL-60 cells, treatment of anisomysin activated JNK pathway activity which further induced cell apoptosis [5]. When tested with primary murine embryonic fibroblasts, anisomycin treatment stimulated cell apoptosis via activating JNK expression [6].

References:
[1].  Jiang, J., et al., Spermassociated antigen 9 promotes astrocytoma cell invasion through the upregulation of podocalyxin. Mol Med Rep, 2014. 10(1): p. 417-22.
[2].  Lin, A., Activation of the JNK signaling pathway: breaking the brake on apoptosis. Bioessays, 2003. 25(1): p. 17-24.
[3].  Liu, J. and A. Lin, Role of JNK activation in apoptosis: a double-edged sword. Cell Res, 2005. 15(1): p. 36-42.
[4].  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.
[5].  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.
[6].  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.