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| 1 | Apoptosis of crypt epithelial cells in ulcerative colitis显示文摘 | Michiko J Takehiko K Kazuya M | 1996 | J Pathol1996，180，2： | 1 |
| 2 | Apoptosis of crypt epithelial cells in ulcerative colitis显示文摘 | MICHIKO J TAKEHIKO K KAZUYA M | 1996 | J Pathol1996，180，： | 1 |
| 3 | Inhibitory effect of yunnan traditional medicines on hepatitis C viral polymerase显示文摘 | MICHIKO J NORIO N NOBUKO K | 2006 | Nat Med2006，60，4： | 1 |
| 4 | 葡萄糖转运的胰岛素敏感性以及forskolin,dipyridamole和pentobarbital对三种L6骨骼肌细胞葡萄糖转运的抑制作用显示文摘用稳定过表达并带有myc表位的葡萄糖转运子1(glucose transporter1,GLUT1)或葡萄糖转运子4(glucose transporter4,GLUT4)的L6骨骼肌细胞株定征GLUT1和GLUT4对胰岛素的响应.所筛选的L6-GLUT1myc细胞克隆分化前后的葡萄糖摄取量均在线性范围.100nmol/L胰岛素使L6-GLUT1myc和L6-GLUT4myc肌原细胞膜上GLUT1或GLUT4的量分别达到基础组的(1.58±0.01)倍和(1.96±0.11)倍,2-脱氧葡萄糖摄取量分别达到了(1.53±0.09)倍和(1.86±0.17)倍,此作用可被渥曼青霉素(wortmannin)抑制.胰岛素刺激了此2种细胞中的Akt磷酸化.L6-GLUT1myc肌原细胞的葡萄糖摄取量对胰岛素浓度呈剂量依赖性,但与野生型细胞相比,其对胰岛素的敏感性和最大响应没有改变.但L6-GLUT4myc肌原细胞的葡萄糖摄取量对胰岛素的敏感性和最大响应均增加.以前的研究提示毛喉素(forskolin)可能影响胰岛素刺激的GLUT4转位.本研究表明,在L6-GLUT4myc细胞中,毛喉素使胰岛素刺激的葡萄糖摄取减少了65%,此作用是由它对GLUT4的直接抑制而不是由其对GLUT4转位的影响造成的.毛喉素和dipyridamole对GLUT4比对GLUT1有更强的抑制作用,而戊巴比妥(pentobarbital)对GLUT1的抑制作用强于GLUT4.应用这些抑制剂的结果表明、L6肌原细胞中基础状态下和胰岛素刺激状态下的葡萄糖主要由过表达的GLUT1或GLUT4转运.因此,L6-GLUT1myc和L6-GLUT4myc细胞株为筛查对肌肉细胞GLUT1或GLUT4的活性或转位有不同作用的化合物提供了一个平台. | 牛文彦 Philip J Bilan Michiko Hayashi 笪宇蓉 姚智 | 2007 | 中国科学(C辑)2007，37，4： | 0 |
| 5 | Insulin sensitivity and inhibition by forskolin,dipyridamole and pentobarbital of glucose transport in three L6 muscle cell lines显示文摘L6 skeletal muscle myoblasts stably overexpressing glucose transporter GLUT1 or GLUT4 with exofa- cial myc-epitope tags were characterized for their response to insulin. In clonally selected cultures, 2-deoxyglucose uptake into L6-GLUT1myc myoblasts and myotubes was linear within the time of study. In L6-GLUT1myc and L6-GLUT4myc myoblasts, 100 nmol/L insulin treatment increased the GLUT1 content of the plasma membrane by 1.58±0.01 fold and the GLUT4 content 1.96±0.11 fold, as well as the 2-deoxyglucose uptake 1.53±0.09 and 1.86±0.17 fold respectively, all by a wortmannin-inhibitable manner. The phosphorylation of Akt in these two cell lines was increased by insulin. L6-GLUT1myc myoblasts showed a dose-dependent stimulation of glucose uptake by insulin, with unaltered sensitiv- ity and maximal responsiveness compared with wild type cells. By contrast, the improved insulin re- sponsiveness and sensitivity of glucose uptake were observed in L6-GLUT4myc myoblasts. Earlier studies indicated that forskolin might affect insulin-stimulated GLUT4 translocation. A 65% decrease of insulin-stimulated 2-deoxyglucose uptake in GLUT4myc cells was not due to an effect on GLUT4 mobi- lization to the plasma membrane, but instead on direct inhibition of GLUT4. Forskolin and dipyridamole are more potent inhibitors of GLUT4 than GLUT1. Alternatively, pentobarbital inhibits GLUT1 more than GLUT4. The use of these inhibitors confirmed that the overexpressed GLUT1 or GLUT4 are the major functional glucose transporters in unstimulated and insulin-stimulated L6 myoblasts. Therefore, L6-GLUT1myc and L6-GLUT4myc cells provide a platform to screen compounds that may have differ- ential effects on GLUT isoform activity or may influence GLUT isoform mobilization to the cell surface of muscle cells. | Philip J BILAN Michiko HAYASHI | 2007 | Science China(Life Sciences)2007，50，6： | 0 |
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