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Brefeldin A

简要描述:Brefeldin A是一种内酯抗生素和ATPase抑制剂,作用于蛋白质转运,在HCT 116细胞中IC50为0.2μM,诱导癌细胞分化和凋亡。BrefeldinA是一种真菌代谢产物,抑制内质网和高尔基体之间的传输,BrefeldinA导致膜蛋白分布受损。

  • 产品型号:abs810012
  • 厂商性质:生产厂家
  • 更新时间:2021-12-19
  • 访  问  量:57

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应用领域化工,生物产业,能源
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描述

Brefeldin A布雷菲德菌素A(BrefeldinA)是一种内酯抗生素和ATPase抑制剂,作用于蛋白质转运,在HCT 116细胞中IC50为0.2μM,诱导癌细胞分化和凋亡。BrefeldinA是一种真菌代谢产物,抑制内质网和高尔基体之间的传输,BrefeldinA导致膜蛋白分布受损。BrefeldinA作用于肿瘤细胞,主要通过诱导分化和凋亡而发挥其细胞毒性作用。

纯度
HPLC>98%
储存/保存方法
Store at -20℃ for one year(Powder);Store at 2-4℃ for two weeks;Store at -20℃ for six months after dissolution.
基本信息
别名
Brefeldin A布雷菲德菌素a; Cyanein; Decumbin; Nectrolide; BFA; Synergisidin
外观
白色或类白色粉末
可溶性/溶解性
DMSO : 14 mg/mL (50 mM)

Ethanol : 2.8 mg/mL (10 mM)
生物活性
靶点
ATPase (HCT 116)
In vitro(体外研究)
Brefeldin A is a fungal metabolite and blocks the forward transport between the endoplasmic reticulum and Golgi apparatus, Brefeldin A causes an impaired distribution of the membrane proteins. When HCT 116 human colon cancer cell is treated with Brefeldin A, morphological changes indicating cell differentiation are observed. Brefeldin A exerts its cytotoxic effects mainly by inducing differentiation and apoptosis in tumor cells. The treatment of the strips with 20 μg/mL Brefeldin A for 6 hours completely abolishes the relaxation induced by bradykinin in the presence of 10mM indomethacin and 30 μM L-NOARG. The treatment with 20 μg/mL Brefeldin A substantially abolishes the bradykinin-induced decreases in i and tension in the range of concentrations between 1 nM and 1 mM. Brefeldin A has no effect on the i elevation in endothelial cells induced by bradykinin or substance P. Addition of the fungal metabolite Brefeldin A does not affect the spontaneous phospholipid-dependent GTPS binding to myr-rARF1 but totally abolishs the retinal isotonic extract (RIE)-catalyzed exchange, with half-maximal inhibition at 2 μM Brefeldin A. Brefeldin A prevents a wide variety of membrane traffic pathways. Brefeldin A inhibits an ADP-ribosylation factor-specific guanine nucleotide exchange activity present in Golgi membranes or in brain cytosol. The complete prevention by Brefeldin A strongly suggests that the retinal extract contains an ARF-specific guanine nucleotide exchange factor. Retinal isotonic extract (RIE)-catalyzed GTPS release from both ADP-ribosylation factors (ARFs) is only partly inhibited by Brefeldin A, even at 300 μM. Brefeldin A induces fusion of the Golgi apparatus with the ER. Brefeldin A abolishes the inhibitory effect of the CERT inhibitor HPA-12. Brefeldin A treatment, which induces fusion of the Golgi apparatus and the ER, rescues the limonoid-induced prevention of sphingomyelin biosynthesis. BFA treatment of CHO cells causes a 2 to 3 fold increase in sphingomyelin synthesis. Apart from B-CLL cells, Brefeldin A reportedly causes apoptosis in multiple myeloma (U266, NCI-H929), Jurkat, HeLa, leukaemia (HL60, K562, BJAB), colon (HT-29) and prostate, as well as adenoid cystic sarcoma cells. The administration of 25 ng/mL of Brefeldin A completely blocks growth of HF4.9 and HF28RA cells, whereas higher Brefeldin A doses (75 ng/mL) are required to achieve the same effect in HF1A3 cells. Cell proliferation is inhibited within 24 hours in a dose-dependent manner and, depending on the cell line, almost complete cessation of 3H-thymdine incorporation is observed at 50-75 ng/mL of Brefeldin A (26%, 76%, 87% inhibition at 50 ng/ml and 75%, 87%, 92% inhibition at 75 ng/mL for HF1A3, HF4.9 and HF28RA cells respectively. Brefeldin A-induced cell killing is in a dose-dependent manner using YO-PRO 1/PI assay. Brefeldin A could improve the HDR(homology-directed repair) efficiency. It is an enhancer of CRISPR-mediated HDR.
参考文献
参考文献
[1] Zhu JW, et al. Bioorg Med Chem. 2000, 8(2), 455-463.
[2] Ohnishi Y, et al. Br J Pharmacol. 2001, 134(1), 168-178.
[3] Franco M, et al. J Biol Chem. 1996, 271(3), 1573-1578.
[4] Hullin-Matsuda F, et al. J Biol Chem. 2012.
[5] Wlodkowic D, et al. Leuk Res. 2007, 31(12), 1687-1700.
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