摘要
目的 :研究 γ射线诱发小鼠白血病模型中 p16基因的失活机制。 方法 :应用聚合酶链反应 (PCR)扩增 39例 γ射线诱发的白血病和对照小鼠胸腺组织中 p16基因第 1、第 2外显子 ,检测等位基因纯合性缺失 ;用限制性内切酶 - PCR法检测p16基因的甲基化发生情况 ;并应用 PCR-单链构象多态性分析银染方法检测 p16基因碱基突变的发生。结果 :在白血病模型中 ,外显子 2的缺失率为 33.3% ,甲基化的发生率为 2 3.1%。 结论 :γ射线诱发的小鼠白血病模型发生、发展过程中伴有 p16基因的改变 。
Objective: To investigate the mechanism of p16 gene inactivation in the mice leukemia model induced by γ ray irradiation.Methods: PCR technique was used to amplify exon 1 and 2 of p16 gene and to detect the homozygous deletion.The occurrence of methylation in the 5′CpG island was studied with restriction enzyme PCR.PCR SSCP silver staining technique was used to detect mutation of p 16 gene.Results: The deletion rate of the exon 2 and the methylation of CpG island in mice leukemia model were 33.3% and 23.1% respectively.Conclusion: The alteration of p16 gene is involved in the development of the mice leukemia induced by γ ray irradiation.The homozygous deletion and methylation are the main manners accounting for inactivation of p16 gene in mice.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
2003年第7期724-727,共4页
Academic Journal of Second Military Medical University
基金
This work is supported by the National NaturalScience F oundation of China ( No.3 0 170 2 82 )