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Anisomycin

茴香霉素
Catalog No.
B6674
JNK激动剂
组合的产品项目
规格价格库存 数量
10mM (in 1mL DMSO)
¥ 454.00
现货
10mg
¥ 454.00
现货
50mg
¥ 909.00
现货

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A

背景

Anisomycin是JNK特异性的激动剂,作用浓度为25 ng / ml[1]。

JNK是c-Jun N端激酶的缩写,作为促凋亡激酶,在许多细胞进程例如细胞周期、增殖、凋亡和细胞应激中起重要作用。研究表明,JNK在UV诱导的细胞凋亡中发挥重要作用,JNK途径的激活可以加强TNF-α介导的细胞凋亡,因此,JNK被认为是临床的重要靶标[2,3]。

Anisomycin是一种强效的JNK激动剂。在细胞系DU145(对Fas介导的凋亡具有较高抗性)中,250 ng/ml anisomysin和Fas (200 ng/ml)共同作用通过激活JNK,诱导DU145细胞凋亡[4]。在HL-60细胞中,使用anisomysin活化JNK途径可以诱导细胞凋亡[5]。在原代鼠胚胎成纤维细胞中,anisomycin通过激活JNK的表达诱导细胞凋亡[6]。

参考文献:
[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.

文献引用

化学属性

Physical AppearanceA solid
StorageStore at -20°C
M.Wt265.31
Cas No.22862-76-6
FormulaC14H19NO4
Solubility≥26.5 mg/mL in DMSO; insoluble in H2O; ≥30.55 mg/mL in EtOH
Chemical Name(2R,3S,4S)-4-hydroxy-2-(4-methoxybenzyl)pyrrolidin-3-yl acetate
SDFDownload SDF
Canonical SMILESO[C@@H]1[C@H]([C@@H](CC(C=C2)=CC=C2OC)NC1)OC(C)=O
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试验操作

Cell experiment:[1]

Cell lines

Hormone refractory cell line DU 145

Reaction Conditions

250 ng/ml anisomycin for 8 h incubation

Applications

In DU 145 cells, anisomycin activated JNK, and acted in synergy with anti-Fas IgM to induce apoptosis. Furthermore, anisomycin was found to activate JNK activation over a prolonged period, whilst anti-Fas IgM was unable to induce transient (1 h) or prolonged (8 h) JNK activation in DU 145 cells.

Animal experiment:[2]

Animal models

Ehrlich ascites carcinoma (EAC)-bearing mice

Dosage form

5 mg/kg

Injected peritumorally every other day for 7 times

Applications

Peritumoral administration of anisomycin (5 mg/kg) significantly suppressed EAC growth, resulting in the survival of approximately 60% of the mice 90 days after EAC inoculation. Enhancement of infiltrating lymphocytes was noted in the tumor tissue, which was dramatically superior to adriamycin.

Note

The technical data provided above is for reference only.

References:

1. Curtin JF, Cotter TG. Anisomycin activates JNK and sensitises DU 145 prostate carcinoma cells to Fas mediated apoptosis. British Journal of Cancer, 2002, 87(10): 1188-1194.

2. You P, Xing F, Huo J, et al. In vitro and in vivo evaluation of anisomycin against Ehrlich ascites carcinoma. Oncology Reports, 2013, 29(6): 2227-2236.

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