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                布雷菲德菌素A;20350-15-6

                簡要描述:布雷菲德菌素A;20350-15-6是一種內酯抗生素和ATPase抑制劑,作用于蛋白質轉運,在HCT 116細胞中IC50為0.2μM,誘導癌細胞分化和凋亡。作用于腫瘤細胞,主要通過誘導分化和凋亡而發揮其細胞毒性作用。

                • 產品型號:abs810012
                • 廠商性質:生產廠家
                • 更新時間:2025-06-10
                • 訪  問  量:1518

                詳細介紹

                品牌absinCAS20350-15-6
                分子式C16H24O4純度HPLC>98%
                分子量280.36貨號abs810012
                規格10mg;25mg供貨周期現貨
                主要用途主要通過誘導分化和凋亡而發揮其細胞毒性作用應用領域化工,生物產業,綜合
                產品描述
                描述

                布雷菲德菌素A(BrefeldinA)是一種內酯抗生素和ATPase抑制劑,作用于蛋白質轉運,在HCT 116細胞中IC50為0.2μM,誘導癌細胞分化和凋亡。BrefeldinA是一種真菌代謝產物,抑制內質網和高爾基體之間的傳輸,BrefeldinA導致膜蛋白分布受損。BrefeldinA作用于腫瘤細胞,主要通過誘導分化和凋亡而發揮其細胞毒性作用。

                純度
                HPLC>98%
                儲存/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
                別名
                布雷菲德菌素a; Cyanein; Decumbin; Nectrolide; BFA; Synergisidin
                外觀
                白色或類白色粉末
                可溶性/溶解性
                DMSO : 14 mg/mL (50 mM)

                Ethanol : 2.8 mg/mL (10 mM)
                生物活性
                靶點
                ATPase (HCT 116)
                In vitro(體外研究)
                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.
                參考文獻
                參考文獻
                [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.
                分子結構圖

                溫馨提示:本產品僅作科研實驗使用,不支持臨床等研究


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