CAJ | 학술논문

　　目的为探讨erK1和erK2激酶在依托泊苷所致的Mcf-7细胞dna损伤中的作用。方法通过特殊的小干扰rna（sirna）分别减少了Mcf-7细胞中的erK1和erK2蛋白的表达,即erK1和erK2基因敲除模型,随后通过western blot检测dna损伤修复过程中p53 s15和atMs1981的磷酸化情况。结果依托泊苷呈剂量依赖性诱导Mcf-7细胞中p53 s15磷酸化，erK1和erK2基因敲除组这种作用明显减弱；依托泊苷剂量依赖性诱导Mcf-7细胞中atMs1981磷酸化,而erK1和erK2基因敲出组中这种作用明显减弱。结论我们认为erK1和erK2两种激酶在依托泊苷诱导的Mcf-7细胞dna损伤中均起作用，它们是通过atM所介导的。
　　목적위탐토erK1화erK2격매재의탁박감소치적Mcf-7세포dna손상중적작용。방법통과특수적소간우rna（sirna）분별감소료Mcf-7세포중적erK1화erK2단백적표체,즉erK1화erK2기인고제모형,수후통과western blot검측dna손상수복과정중p53 s15화atMs1981적린산화정황。결과의탁박감정제량의뢰성유도Mcf-7세포중p53 s15린산화，erK1화erK2기인고제조저충작용명현감약；의탁박감제량의뢰성유도Mcf-7세포중atMs1981린산화,이erK1화erK2기인고출조중저충작용명현감약。결론아문인위erK1화erK2량충격매재의탁박감유도적Mcf-7세포dna손상중균기작용，타문시통과atM소개도적。
Objective to determine the contribution of erK1 and erK2 to etoposide-induced G2/M arrest.Methods We individually knocked down ERK1 and ERK2 in MCF-7 cells using specific small interfering RNA(siRNA), than the typical event of dna damage response(ddr),such as p53 s15 and atM1981 were examined by western blot.results etoposide dose-dependently induced p53 S15 phosphorylation in control cells, this event was significantly attenuated when either ERK1 or erK2 was knoced-down.etoposide dose-dependently induced the atM s1981 phosphorylation in ctrl Mcf-7 cells, which was significantly reduced when either ERK1 or ERK2 was knoced-down.Conclusion Both ERK1 and ERK2 kinases plays a roll in etoposide induced ddr, which is mediated by atM.