Thapsigargin 毒胡萝卜素;Sarco/endoplasmic reticulum Ca2+-ATPase (SERCAs) 心肌肌浆网钙ATP酶;Tumor promoter 肿瘤促进剂;Autophagy Inhibitor 自吞噬;CAS NO:67526-95-8;
产品描述
细胞内心肌肌浆网钙ATP酶(SERCAs)运输游离Ca2+进入肌质和内质网,从而降低细胞内Ca2+水平,进而终止Ca2+介导的信号通路。毒胡萝卜素(Thapsigargin,TG)是一种非竞争性、细胞膜渗透性的SERCAs介导的钙离子转运抑制剂(IC50s具细胞类型依赖性,范围约为2-80nM)。对SERCAs的抑制引起胞内Ca2+水平上升,这一变化与细胞活化,肥大细胞组胺释放和某些癌症细胞增殖提高有关联。体内毒胡萝卜素和相关的倍半萜内酯具抗炎症和抗肿瘤效应。
产品特性
1)CAS NO:67526-95-8
2)化学名:(3S,3aS,4R,6R,7S,8R)-6-acetoxy-4-(butyryloxy)-3,3a-dihydroxy-3,6,9-trimethyl-8-(((Z)-2- methylbut-2-enoyl)oxy)-2-oxo-2,3,3a,4,5,6,6a,7,8,9b-decahydro-1H-cyclopenta[e]azulen-7-yl octanoate
3)分子式:C34H50O12
4)分子量:650.8
5)纯度:≥97%
6) 外观:固体或透明薄膜
7) 溶解性:溶于DMSO(~30mg/ml),无水乙醇(~30mg/ml)
8)化学结构图:
保存与运输方法
保存:-20℃干燥保存,至少2年有效。
运输:冰袋运输。
实验数据(文献来源)
[1] Sabała P et al. Thapsigargin: potent inhibitor of Ca2+transport ATP-ases of endoplasmic and sarcoplasmic reticulum.Acta Biochim Pol. 1993;40(3):309-19.
[2] Wang Fet al. Thapsigargin Induces Apoptosis by Impairing Cytoskeleton Dynamics in Human Lung Adenocarcinoma Cells. Scientific World Journal. 2014 Jan 28;2014:619050.
生理功能:A549细胞中Thapsigargin(TG)诱导细胞凋亡,以时间-和剂量-依赖性的方式【见下图】。
[3] Spohn D et al.Thapsigargin induces expression of activating transcription factor 3 in human keratinocytes involving Ca2+ ions and c-Jun N-terminal protein kinase. Mol Pharmacol. 2010 Nov;78(5):865-76.
生理功能:HaCaT细胞经Thapsigargin(TG)刺激后,诱导角化细胞中特定化的信号通路,涉及JNK激活、ATF3生物合成和caspase-3/7活性的上调。
[4] Thastrup Oet al.Thapsigargin, a tumor promoter, discharges intracellular Ca2+ stores by specific inhibition of the endoplasmic reticulum Ca2(+)-ATPase. Proc Natl Acad Sci U S A. 1990 Apr;87(7):2466-70.
[5] Huber Met al.Thapsigargin-Induced Degranulation of Mast Cells Is Dependent on Transient Activation of Phosphatidylinositol-3 Kinase. J Immunol July 1, 2000, 165 (1) 124-133.
[6] Jackisch Cet al.Delayed micromolar elevation in intracellular calcium precedes induction of apoptosis in thapsigargin-treated breast cancer cells. Clin Cancer Res. 2000 Jul;6(7):2844-50.
[7] Ganley IGet al.Distinct autophagosomal-lysosomal fusion mechanism revealed by thapsigargin-induced autophagy arrest. Mol Cell. 2011 Jun 24;42(6):731-43
生理功能:Thapsigargin(TG)阻断自吞噬。作用机制:ER应激源(ER stressor)TG不会影响自噬体形成,但通过阻断自噬体与内吞系统溶酶体的融合引起成熟自噬体的积累(见下图)。
注意事项
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