CAS NO: | 634207-53-7 |
包装 | 价格(元) |
500ug | 电议 |
1mg | 电议 |
5mg | 电议 |
Physical Appearance | White lyophilised solid |
Storage | Desiccate at -20°C |
M.Wt | 507.82 |
Cas No. | 634207-53-7 |
Formula | C17H16ClN5O6PS·Na |
Solubility | <50.78mg/ml in H2O |
Chemical Name | sodium (4aS,6S,7S,7aS)-6-(6-amino-8-((4-chlorophenyl)thio)-9H-purin-9-yl)-7-methoxytetrahydro-4H-furo[3,2-d][1,3,2]dioxaphosphinin-2-olate 2-oxide |
Canonical SMILES | [H][C@]12COP(O[C@]1([H])[C@H](OC)[C@@H](N3C(SC4=CC=C(C=C4)Cl)=NC5=C3N=CN=C5N)O2)(O[Na])=O |
运输条件 | 蓝冰运输或根据您的需求运输。 |
一般建议 | 为了使其更好的溶解,请用37℃加热试管并在超声波水浴中震动片刻。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。 |
8-CPT-2Me-cAMP, sodium salt是EPAC的选择性激动剂[1]。
环AMP鸟嘌呤核苷酸交换因子(EPACs)是cAMP的细胞内传感器,作为Ras GTPase同系物RAP1和RAP2的核苷酸交换因子而起作用[1]。
8-CPT-2Me-cAMP, sodium salt是EPAC的选择性激动剂。8-CPT-2Me-cAMP增加EPAC1对Rap1的激活。同时,微管相关蛋白MAP1A的轻链2(LC2)可增加该反应。在LC2和EPAC1转染细胞中,8-CPT-2Me-cAMP 增加细胞与层粘连蛋白的粘附[1]。在Jurkat T细胞中,8-CPT-2Me-cAMP(100 μM)激活Rap1,该反应不受PKA抑制剂H-89的影响[2]。在1-LN前列腺癌细胞中,8-CPT-2Me-cAMP以剂量依赖的方式增加Epac1、p-AktS473和p-AktT308。8-CPT-2Me-cAMP增加2-3倍的p-AktS473和AktS473激酶活性。8-CPT-2Me-cAMP也激活mTORC1和mTORC2[3]。
在人前列腺癌细胞中,8-CPT-2Me-cAMP增加p-cPLA2S505、COX-2和PGE2的水平。然而,COX-2、EP4或mTOR的抑制剂抑制该效应,减少Epac1诱导的蛋白和DNA合成。这些结果表明Epac1是促炎调制器,促进细胞增殖[4]。
参考文献:
[1]. Gupta M, Yarwood SJ. MAP1A light chain 2 interacts with exchange protein activated by cyclic AMP 1 (EPAC1) to enhance Rap1 GTPase activity and cell adhesion. J Biol Chem, 2005, 280(9): 8109-8116.
[2]. Fuld S, Borland G, Yarwood SJ. Elevation of cyclic AMP in Jurkat T-cells provokes distinct transcriptional responses through the protein kinase A (PKA) and exchange protein activated by cyclic AMP (EPAC) pathways. Exp Cell Res, 2005, 309(1): 161-173.
[3]. Misra UK, Pizzo SV. Upregulation of mTORC2 activation by the selective agonist of EPAC, 8-CPT-2Me-cAMP, in prostate cancer cells: assembly of a multiprotein signaling complex. J Cell Biochem, 2012, 113(5): 1488-1500.
[4]. Misra UK, Pizzo SV. Evidence for a pro-proliferative feedback loop in prostate cancer: the role of Epac1 and COX-2-dependent pathways. PLoS One, 2013, 8(4): e63150.