CAS NO: | 22862-76-6 |
包装 | 价格(元) |
10mM (in 1mL DMSO) | 电议 |
10mg | 电议 |
50mg | 电议 |
Physical Appearance | A solid |
Storage | Store at -20°C |
M.Wt | 265.31 |
Cas No. | 22862-76-6 |
Formula | C14H19NO4 |
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 |
Canonical SMILES | O[C@@H]1[C@H]([C@@H](CC(C=C2)=CC=C2OC)NC1)OC(C)=O |
运输条件 | 蓝冰运输或根据您的需求运输。 |
一般建议 | 为了使其更好的溶解,请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异,仅做参考。若实验所需浓度过大至产品溶解极限,请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存,请尽快用完。 |
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.
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. |