Control of p53-dependent apoptosis by E1B, Bcl-2, and Ha-ras proteins.
Control of p53-dependent apoptosis by E1B, Bcl-2, and Ha-ras proteins.
复制标题
E1B、Bcl-2 和 Ha-ras 蛋白控制 p53 依赖性细胞凋亡。
DOI：
10.1101/sqb.1994.059.01.044
复制
发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Lin,HJ
中科院分区：
文献类型：
--
作者：
White,E;Chiou,SK;Rao,L;Sabbatini,P;Lin,HJ
METHODSPlasmids and tissue culture. Primary Fisher baby rat kidney (BRK) cells were used as a source of primary cells for transformation assays with adenoviral oncogenes E1A and E1B. BRK cells were transfected with plasmid DNAs by electroporation as described previously (White et al. 1991). To derive cell lines that undergo controlled p53-dependent apoptosis, primary BRK cells were transfected with a cytomegalovirus (CMV) promoter construct to express the EIA (pCMVE1A, White et al. 1991) and the plasmid pLTRcGva1135 (Michalovitz et al. 1990) to express murine mutant p53 (va1135). The p53 (va1135) protein is temperature sensitive and predominantly in the mutant conformation at 37.5~ 176 and predominantly in the wild-type conformation at 32~(Michalovitz et al. 1990; Gannon and Lane 1991; Martinez et al. 1991). Continuous propagation of cell lines transformed with
