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作 者:刘宽[1,2] 曾现伟[2,3] 吉训明[1] 刘向荣[1]
机构地区:[1]首都医科大学宣武医院脑血管病研究室,北京100053 [2]潍坊医学院临床学院,山东潍坊261053 [3]潍坊医学院附属医院神经外科,山东潍坊261031
出 处:《临床与病理杂志》2016年第6期859-863,共5页Journal of Clinical and Pathological Research
基 金:国家自然科学基金面上项目(81471209);北京市自然科学基金面上项目(7132112)~~
摘 要:p53凋亡刺激蛋白家族(apoptosis stimulating proteins of p53 family,ASPPs)由ASPP1、ASPP2和i ASPP(inhibitor y member of the ASPP family)3个成员组成,该家族可通过与p53家族(p53/p63/p73)结合,调控细胞凋亡。自噬是细胞通过溶酶体溶解并回收利用胞内物质,藉此以维持自我稳态的一种方式。目前认为,自噬功能紊乱与肿瘤、神经退行性病变等多种疾病的发生和发展密切相关。本综述总结了近期关于ASPPs对自噬调控作用的研究进展,这些研究证明ASPPs能调控细胞内的自噬水平,并提示ASPPs可能成为多种疾病的潜在治疗靶点。The apoptosis stimulating proteins of p53 family(ASPPs) consists of three members, ASPP1, ASPP2 and inhibitory member of the ASPP family(i ASPP), which function is to regulate the apoptotic function of p53 family(p53/p63/p73). Autophagy is a process to degrade and recycle cellular constituents via the lysosome for regulating cellular homeostasis. The dysfunction of autophagy is considered to be involved in the occurrence and progress of many diseases, such as tumors and neurodegenerative diseases. Our current review summarizes the recent reports about the role of ASPPs on autophagy. These studies have identified that ASPPs could regulate the level of intracellular autophagy and suggest that ASPPs might be potential therapeutic targets for various diseases.
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