Atractyloside Dipotassium Salt
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Atractyloside Dipotassium Salt是一种ADP/ATP转位酶抑制剂。
ATP-ADP转位酶(AAT)是一种线粒体ADP/ATP载体。AAT将ATP从线粒体基质转移至细胞质,并将ADP从细胞质转移至线粒体基质。
在艾氏腹水癌细胞中,Atractyloside (3 mM)抑制70%细胞生长。线粒体是球形的,具有去除嵴的半透明基质。当转移到正常介质中时,增殖和大分子合成在3到6 h之内恢复到正常水平[ 2 ]。
在兔骨骼肌的肌浆网泡中,细胞质Ca2+为10 μM, Atractyloside将通过Ca2+ 通道流入的胆碱比率降到60%。此外,Atractyloside抑制了约一半的嵌入膜双分子层的Ca2+ 通道[ 1 ]。在大鼠心肌分离的线粒体膜中,Atractyloside (5-100 μM)剂量依赖性地抑制氯离子通道[ 3 ]。
参考文献:
[1].Yamaguchi N, Kagari T, Kasai M. Inhibition of the ryanodine receptor calcium channel in the sarcoplasmic reticulum of skeletal muscle by an ADP/ATP translocase inhibitor, atractyloside. Biochem Biophys Res Commun, 1999, 258(2): 247-251.
[2].Pick-Kober KH, Schneider F. Proliferation, macromolecular synthesis and energy metabolism of in vitro grown Ehrlich ascites tumor cells after inhibition of ATP-ADP translocation by atractyloside. Eur J Cell Biol, 1984, 34(2): 323-329.
[3].Malekova L, Kominkova V, Ferko M, et al. Bongkrekic acid and atractyloside inhibits chloride channels from mitochondrial membranes of rat heart. Biochim Biophys Acta, 2007, 1767(1): 31-44.
- 1.Zhu H, Ding Y, et al. "Prostaglandin E1 protects coronary microvascular function via the glycogen synthase kinase 3β-mitochondrial permeability transition pore pathway in rat hearts subjected to sodium laurate-induced coronary microembolization." Am J Transl Res. 2017 May 15;9(5):2520-2534. PMID:28560002
Physical Appearance | A crystalline solid |
Storage | Store at -20°C |
M.Wt | 802.99 |
Cas No. | 102130-43-8 |
Formula | C30H44K2O16S2 |
Solubility | ≥37.05 mg/mL in DMSO; ≥51 mg/mL in EtOH; ≥110.4 mg/mL in H2O |
Chemical Name | potassium (2R,3R,4R,5R,6S)-6-(((2aR,3R,5R,6aR,6bS,9R,11S,11aR)-3-carboxy-11-hydroxy-6a-methyl-10-methylenetetradecahydro-9,11a-methanocyclohepta[a]naphthalen-5-yl)oxy)-2-(hydroxymethyl)-5-((3-methylbutanoyl)oxy)tetrahydro-2H-pyran-3,4-diyl bis(sulfate) |
SDF | Download SDF |
Canonical SMILES | CC(C)CC(=O)OC1C(C(C(OC1OC2CC(C3CCC45CC(CCC4C3(C2)C)C(=C)C5O)C(=O)O)CO)OS(=O)(=O)[O-])OS(=O)(=O)[O-].[K+].[K+] |
运输条件 | 蓝冰运输或根据您的需求运输。 |
一般建议 | 不同厂家不同批次产品溶解度各有差异,仅做参考。若实验所需浓度过大至产品溶解极限,请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存,请尽快用完。 |
细胞实验 [1-3]: | |
细胞系 |
Ehrlich腹水肿瘤细胞,J2-3T3细胞和宫颈癌细胞 |
溶解方法 |
该化合物在DMSO中的溶解度大于37.05 mg/mL。若获取更高浓度的溶液,可在37℃下孵育10分钟,随后在超声波浴中摇匀。-20℃以下可储存数月。 |
反应条件 |
3 mM,24 h |
应用 |
在培养的Ehrlich腹水肿瘤细胞中,atractyloside(3 mM,24 h)抑制70%的细胞生长,对细胞活力没有严重的影响。Atractyloside延迟细胞周期进程。将Atractyloside处理的细胞转移至正常培养基后,细胞增殖和大分子合成在3-6小时内恢复正常。Atractyloside增加葡萄糖消耗和乳酸产生,24小时后乳酸/葡萄糖比为1.9。Atractyloside减少氧气摄取。Atractyloside增加线粒体和线粒体室内的ATP/ADP浓度比。在正常的J2-3T3细胞和宫颈癌细胞中,Atractyloside通过诱导细胞活力丧失、核碎裂和DNA梯度,以剂量依赖性方式诱导细胞凋亡。细胞对Atractyloside诱导的凋亡敏感性为:HPV16 E6-J2-3T3>CaSki>正常J2-3T3细胞≈ts p53-J2-3T3≈载体-J2-3T3细胞> Hela > SiHa > C33A≈C33A 16 E6。在小动脉平滑肌细胞(ASMC)中,Atractyloside诱导线粒体通透性转换孔(mPTP)的开放。用7.5、10和15 μM atractyloside处理10分钟,ASMCs中相对ATP的含量降低48%、63%和66%,ASMCs处于超极化状态。 |
注意事项 |
由于实验环境的不同,实际溶解度可能与理论值略有不同,请测试室内所有化合物的溶解度。 |
References: [1]. Pick-Kober K H, Schneider F. Proliferation, macromolecular synthesis and energy metabolism of in vitro grown Ehrlich ascites tumor cells after inhibition of ATP-ADP translocation by atractyloside[J]. European journal of cell biology, 1984, 34(2): 323-329. [2]. Brown J, Higo H, Mckalip A, et al. Human papillomavirus (HPV) 16 E6 sensitizes cells to atractyloside‐induced apoptosis: Role of p53, ICE‐like proteases and the mitochondrial permeability transition[J]. Journal of cellular biochemistry, 1997, 66(2): 245-255. [3]. Song R, Bian H, Huang X, et al. Atractyloside induces low contractile reaction of arteriolar smooth muscle through mitochondrial damage[J]. Journal of Applied Toxicology, 2012, 32(6): 402-408. |
质量控制和MSDS
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