EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #73682_C
鞘脂合成和蛋白丝氨酸/苏氨酸磷酸酶抑制剂
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总览
Fumonisin B1（伏马菌素B1）是由串珠镰刀菌（Fusarium moniliforme）产生的一种霉菌毒素，已被证明能强效抑制鞘氨醇N-酰基转移酶（神经酰胺合酶；Wang et al.），从而干扰鞘脂（质膜的关键成分）的合成（IC₅₀=0.1 µM）。伏马菌素B1还能抑制蛋白丝氨酸/苏氨酸磷酸酶（PPs；PP1、PP2A、PP2B、PP2C和PP5/T/K/H），IC₅₀值为80-3000 μM。PP5最敏感，IC₅₀值为80 μM（Fukuda et al.）。伏马菌素B1与黄曲霉毒素B1协同作用，可增加大鼠脾细胞的活性氧水平和氧化损伤（Mary et al.）。
维持培养与自我更新
·可逆地阻止瑞士3T3细胞的细胞增殖和DNA合成（Meivar-Levy et al.）。
·阻止十六烷基磷酸胆碱（HePC）诱导的人角质形成细胞系细胞凋亡（Wieder et al.）。
分化
·破坏小脑浦肯野神经元的树突生长（Furuya et al）。
·抑制培养的海马神经元的轴突分支（Schwarz et al.）。
癌症研究
·减弱小鼠淋巴瘤细胞系对血小板活化因子的反应，并通过抑制神经酰胺形成来阻止HePC诱导的细胞凋亡（Balsinde et al.）。
细胞类型
癌细胞及细胞系，角质形成细胞，白血病/淋巴瘤细胞，神经元
种属
人，小鼠，非人灵长类，其它细胞系，大鼠
应用
分化
研究领域
癌症，神经科学
CAS 编号
116355-83-0
化学式
C₃₄H₅₉NO₁₅
纯度
≥ 95 %
靶点
鞘氨醇N-酰基转移酶
产品说明书及文档
请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。
相关材料与文献
文献 (8)
Reactive oxygen species sources and biomolecular oxidative damage induced by aflatoxin B1 and fumonisin B1 in rat spleen mononuclear cells. Toxicology 2012 DEC
Abstract
Aflatoxin B1 (AFB(1)) and fumonisin B1 (FB(1)) are mycotoxins widely found as cereal contaminants. Their immunotoxicities predispose to infectious diseases and may alter the tumor immunosurveillance of human and animals, but the mechanisms underlying have not been fully elucidated, and the induction of oxidative stress has been proposed as a probable mechanism. This work was aimed at evaluating in spleen mononuclear cells (SMC) from Wistar rats the effects of the exposure, in vitro for up to 48 h, to 20 μM AFB(1), 10 μM FB(1) and AFB(1)-FB(1) mixture (MIX), over cellular oxidative status, as well as at elucidating the contribution of different reactive oxygen species (ROS) to biomolecular oxidative damage, the biochemical pathways involved, and the probable interaction of both toxins to induce oxidative stress. All the treatments increased total ROS and oxidation of biomolecules, with MIX having the greatest effects. However, only MIX increased superoxide anion radical. The main ROS involved in oxidation of proteins, lipids and DNA appear to be hydrogen peroxide and hydroxyl radical. The mitochondrial complex I and CYP450 were involved in the ROS generation induced by all treatments. The NADPH oxidase system was induced by FB1 and MIX. The arachidonic acid metabolism contributed to the ROS formation induced by AFB(1) and MIX. These results demonstrate that an interaction between AFB(1) and FB(1) occur in the oxidative stress induction, and show the biochemical pathways involved in ROS generation in SMC. The oxidative stress could mediate the AFB(1) and FB(1) individual and combined immunotoxicities.
Induction of ceramide-mediated apoptosis by the anticancer phospholipid analog, hexadecylphosphocholine. The Journal of biological chemistry 1998 MAY
Abstract
The prototype of a new class of antiproliferative phospholipid analogs, hexadecylphosphocholine (HePC), has been shown to inhibit tumor growth and is currently used for the treatment of cutaneous metastases of mammary carcinomas. Although several cellular targets of HePC, e.g. protein kinase C and CTP:phosphocholine cytidylyltransferase, have been proposed, the mechanisms of HePC-induced anticancer activity are still unclear. Considering that the antiproliferative effect of HePC correlates with inhibition of phosphatidylcholine biosynthesis, which is tightly coupled to sphingomyelin biosynthesis, we tested the hypothesis that treatment of cells with the anticancer drug leads to increased cellular ceramide and subsequently to apoptotic cell death. In the present study, we showed that 25 micromol/liter HePC induced apoptosis. In further experiments, we demonstrated that HePC inhibited the incorporation of radiolabeled choline into phosphatidylcholine and at a later time point into sphingomyelin. This was confirmed by metabolic labeling of the lipid backbone using radiolabeled serine, and it was shown that HePC decreased the incorporation of serine into sphingomyelin by 35% and simultaneously increased the incorporation of serine into ceramide by 70%. Determination of the amount of ceramide revealed an increase of 53% in HePC-treated cells compared with controls. In accordance with the hypothesis that elevated ceramide levels may be the missing link between the metabolic effects of HePC and its proapoptotic properties, HePC-induced apoptosis was blocked by fumonisin B1, an inhibitor of ceramide synthesis. Furthermore, we found that membrane-permeable ceramides additively increased the apoptotic effect of HePC.
The role of sphingolipids in the maintenance of fibroblast morphology. The inhibition of protrusional activity, cell spreading, and cytokinesis induced by fumonisin B1 can be reversed by ganglioside GM3. The Journal of biological chemistry 1997 JAN
Abstract
Previous studies demonstrated that inhibition of sphingolipid synthesis by the mycotoxin fumonisin B1 (FB1) disrupts axonal growth in cultured hippocampal neurons (Harel, R., and Futerman, A. H. (1993) J. Biol. Chem. 268, 14476-14481) by affecting the formation or stabilization of axonal branches (Schwarz, A., Rapaport, E., Hirschberg, K., and Futerman, A.H. (1995) J. Biol. Chem. 270, 10990-10998). We now demonstrate that long term incubation with FB1 affects fibroblast morphology and proliferation. Incubation of Swiss 3T3 cells with FB1 resulted in a decrease in synthesis of ganglioside GM3, the major glycosphingolipid in 3T3 fibroblasts and of sphingomyelin. The projected cell area of FB1-treated cells was approximately 45% less than control cells. FB1 had no affect on the organization of microtubules or intermediate filaments, but fewer actin-rich stress fibers were observed, and there was a loss of actin-rich lamellipodia at the leading edge. Three other processes involving the actin cytoskeleton, cytokinesis, microvilli formation, and the formation of long processes induced by protein kinase inhibitors, were all disrupted by FB1. All the effects of FB1 on cell morphology could be reversed by addition of ganglioside GM3 even in the presence of FB1, whereas the bioactive intermediates, sphinganine, sphingosine, and ceramide, were without effect. Finally, FB1 blocked cell proliferation and DNA synthesis in a reversible manner, although ganglioside GM3 could not reverse the effects of FB1 on cell proliferation. Together, these data suggest that ongoing sphingolipid synthesis is required for the assembly of both new membrane and of the underlying cytoskeleton.
更多信息
| 种属 | Human, Mouse, Non-Human Primate, Other, Rat |
|---|---|
| Cas Number | 116355-83-0 |
| Chemical Formula | C₃₄H₅₉NO₁₅ |
| 纯度 | ≥ 95% |
| Target | Sphingosine N-Acyltransferase |
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质量保证:
产品仅供研究使用，不用于针对人或动物的诊断或治疗。 欲获悉更多关于STEMCELL的质控信息，请访问 STEMCELL.CN/COMPLIANCE. Safety Statement: CA WARNING: This product can expose you to Fumonisin B1 which is known to the State of California to cause cancer. For more information go to www.P65Warnings.ca.gov
产品仅供研究使用，不用于针对人或动物的诊断或治疗。 欲获悉更多关于STEMCELL的质控信息，请访问 STEMCELL.CN/COMPLIANCE. Safety Statement: CA WARNING: This product can expose you to Fumonisin B1 which is known to the State of California to cause cancer. For more information go to www.P65Warnings.ca.gov
