| 供货周期： | 一周 |
| 品牌： | 爱必信 |
| 规格： | ＞98% |
| 货号： | abs816918 |
| CAS号： | 474-25-9 |
| 公告提醒：爱必信所有产品和服务仅用于科学研究，不用于临床应用及其他用途提供产品和服务（也不为任何个人提供产品和服务）!
抑制剂描述： 产品名称：Chenodeoxycholic acid 产品别名：见爱必信官网 英文别名：Chenodeoxycholic acid 靶点：Steroids CAS：474-25-9 纯度：＞98% 外观：见爱必信官网 保存方法：store at -20℃ for one year（Powder）； in DMSO or others solvent store at 2-4℃ for two weeks, at -20℃ for six months. 描述： Chenodeoxycholic Acid (CDCA), is a hydrophobic primary bile acid that activates nuclear receptors(FXR) involved in cholesterol metabolism. 溶解性：DMSO : ≥ 50 mg/mL (127.37 mM) 体外研究： Chenodeoxycholic acid (CDCA) and Deoxycholic acid (DCA) both inhibits 11 beta HSD2 with IC(50) values of 22 mM and 38 mM, respectively and causes cortisol-dependent nuclear translocation and increases transcriptionalactivity of mineralocorticoid receptor (MR). Chenodeoxycholic acid is able to stimulate Ishikawa cell growth by inducing a significant increase in Cyclin D1 protein and mRNA expression through the activation of the membrane G protein-coupled receptor (TGR5)-dependent pathway. Chenodeoxycholic acid (CDCA) induces LDL receptor mRNA levels approximately 4 fold and mRNA levels for HMG-CoA reductase and HMG-CoA synthase two fold in a cultured human hepatoblastoma cell line, Hep G2. Chenodeoxycholic acid-induced Isc is inhibited (≥67%) by Bumetanide, BaCl2, and the cystic fibrosis transmembrane conductance regulator (CFTR) inhibitor CFTRinh-172. Chenodeoxycholic acid-stimulated Isc is decreased 43% by the adenylate cyclase inhibitor MDL12330A and Chenodeoxycholic acid increases intracellular cAMP concentration. Chenodeoxycholic acid treatment activates C/EBPβ, as shown by increases in its phosphorylation, nuclear accumulation, and expression in HepG2 cells. Chenodeoxycholic acid enhances luciferase gene transcription from the construct containing -1.65-kb GSTA2 promoter, which contains C/EBP response element (pGL-1651). Chenodeoxycholic acid treatment activates AMP-activated protein kinase (AMPK), which leads to extracellular signal-regulated kinase 1/2 (ERK1/2) activation, as evidenced by the results of experiments using a dominant-negative mutant of AMPKα and chemical inhibitor. 体内研究：
产品信息订购：
|
相关产品
工商信息
信息已认证
联系方式
详细地址
关注
拨打电话
留言咨询
