T型钙通道在表达Cav3.1的HEK293细胞中触发p21ras信号通路至ERK。
T-type calcium channel trigger p21ras signaling pathway to ERK in Cav3.1-expressed HEK293 cells.
作者信息
Choi Juhyun, Park Jong-Hwa, Kwon Oh Yeun, Kim Sunoh, Chung Ji Hyung, Lim Dae Sik, Kim Key Sun, Rhim Hyewhon, Han Ye Sun
机构信息
Biomedical Research Center, Korea Institute of Science and Technology, Seoul, Korea.
出版信息
Brain Res. 2005 Aug 23;1054(1):22-9. doi: 10.1016/j.brainres.2005.05.010.
We constructed a new cell line which stably expressed Cav3.1 and Kir2.1 subunits in HEK293 cells (HEK293/Cav3.1/Kir2.1) in order to investigate the unknown cellular signaling pathways of T-type voltage-dependent calcium channels. The new cell line has a stable resting membrane potential and can activate T-type Ca(2+) channels by KCl-mediated depolarization. We showed that Cav3.1 activation resulted in the level of p21(ras)-GTP in the cells being rapidly decreased during the first 2 min, and then recovering between 2 min and 15 min. The kinetics of ERK activation following Cav3.1 stimulation was also investigated. ERK activation was decreased from 2 min to 5 min after KCl stimulation, which means that Cav3.1 activation reduced ERK activity in the very early stages of activation. In addition, similar results for Cav3.1 activation were also shown in the case of Sos1, Grb2, and Shc, which means that Cav3.1 activation triggers p21(ras) and that this signal is transferred to ERK by Sos1, Grb2, and Shc.
为了研究T型电压依赖性钙通道未知的细胞信号通路，我们构建了一种在HEK293细胞（HEK293/Cav3.1/Kir2.1）中稳定表达Cav3.1和Kir2.1亚基的新细胞系。该新细胞系具有稳定的静息膜电位，并且可以通过KCl介导的去极化激活T型Ca(2+)通道。我们发现，Cav3.1激活导致细胞中p21(ras)-GTP水平在最初2分钟内迅速下降，然后在2分钟至15分钟之间恢复。我们还研究了Cav3.1刺激后ERK激活的动力学。KCl刺激后2分钟至5分钟ERK激活降低，这意味着Cav3.1激活在激活的早期阶段降低了ERK活性。此外，在Sos1、Grb2和Shc的情况下也显示了Cav3.1激活的类似结果，这意味着Cav3.1激活触发p21(ras)，并且该信号通过Sos1、Grb2和Shc传递至ERK。
Zotero 插件