遗传 ›› 2012, Vol. 34 ›› Issue (12): 1513-1521.doi: 10.3724/SP.J.1005.2012.01513
魏永永, 侯静, 唐文如, 罗瑛
收稿日期:
2012-04-16
修回日期:
2012-06-02
出版日期:
2012-12-20
发布日期:
2012-12-25
通讯作者:
罗瑛
E-mail:luoyingabc@yahoo.com
基金资助:
国家自然科学基金项目(编号:31170735, 81101547)和教育部新世纪优秀人才项目资助
WEI Yong-Yong, HOU Jing, TANG Wen-Ru, LUO Ying
Received:
2012-04-16
Revised:
2012-06-02
Online:
2012-12-20
Published:
2012-12-25
摘要: 肿瘤发生是抑癌基因失活和原癌基因激活共同作用的结果。p53基因被认为是目前最重要的抑癌基因, 50%以上的肿瘤中存在p53基因的点突变现象; 而Ras基因是肿瘤中突变率较高的原癌基因, 其突变率在某些肿瘤中高达30%~90%。研究发现, 肿瘤发生过程中抑癌基因p53与原癌基因Ras之间存在复杂的相互协同作用。根据目前的文献报道, p53与Ras之间的协同作用可以分为3种:第一, p53对Ras的调节作用; 第二, Ras对p53的调节作用; 第三, p53和Ras共同调控某些与肿瘤发生相关的关键基因。了解p53与Ras之间的3种调控作用将有助于我们进一步认识p53失活与Ras激活协同促进肿瘤发生的分子通路和机制, 同时也将为癌症的个性化治疗和药物靶点的选择提供重要依据。因此, 文章将对近年来所发现的p53与Ras的各种协同作用机制及其与肿瘤发生的关系进行概括和综述。
魏永永,侯静,唐文如,罗瑛. p53与Ras协同及其在肿瘤发生中的作用[J]. 遗传, 2012, 34(12): 1513-1521.
WEI Yong-Yong HOU Jing TANG Wen-Ru LUO Ying. The cooperation between p53 and Ras in tumori-genesis[J]. HEREDITAS, 2012, 34(12): 1513-1521.
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