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在色谱分析、有机合成和交叉偶联反应领域已被 7 篇同行评审文献引用。
Brefeldin A可溶于DMSO(20mg/ml),乙醇(5mg/ml)和甲醇(10mg/ml)。 使用说明: 1. Brefeldin A常见使用浓度范围为1-50μM。具体的最佳工作浓度请参考相关文献,或根据实验目的,以及所培养的特定细 胞和组织,通过实验进行摸索和优化。Brefeldin A,是一种常用的蛋白转运抑制剂,特异性地可逆地阻断蛋白质从内质网(ER)转运到高尔基体 (Golgi)。Brefeldin A处理后,高尔基体会很快被破坏,并融合到内质网上,该过程呈现能量、温度和微管依赖性。在哺乳动物和酵母中,Brefeldin A对蛋白从内质网向高尔基体转运的抑制可能是通过一类可以激活Afr1p GTPase的GTP-exchange factors来实现的。Arf1p在通过招募coat proteins到细胞内膜形成转运小泡(transport vesicles)的过程中起重要作用。Brefeldin A是一种真菌代谢产物,最初曾被用作抗病毒试剂,现在主要用于研究蛋白转运。Brefeldin A也常被用于抑制细胞因子等蛋白的分泌,并用于增强分泌蛋白的免疫染色检测。Brefeldin A 可激活神经鞘磷脂循环(sphingomyelin cycle),还可诱导一些肿瘤细胞发生凋亡。
Information
Brefeldin A Brefeldin A is a lactone antibiotic and ATPase inhibitor for protein transport with IC50 of 0.2 μM in HCT 116 cells, induces cancer cell differentiation and apoptosis . It could also improve the HDR(homology-directed repair) efficiency and b
In vitro
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 [Ca2+]i and tension in the range of concentrations between 1 nM and 1 mM. Brefeldin A has no effect on the [Ca2+]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.
In vivo
Cell Data
cell lines:
Concentrations:0 ng/mL -75 ng/mL
Incubation Time:5 days
Powder Purity:≥99%
H301: 吞咽会中毒
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| 批号(Lot Number) | 证书类型 | 货号 |
|---|---|---|
| 分析证书 | B408392 |