Post-translational modification of Parkin and its research progress in cancer  

作　　者：Dan Ding Xiang Ao Ying Liu Yuan-Yong Wang Hong-Ge Fa Meng-Yu Wang Yu-Qi He Jian-Xun Wang 

机构地区：[1]School of Basic Medical Sciences,Qingdao University,No.38 Dengzhou Road,Shibei District,Qingdao 266000,Shandong,P.R.China [2]Center for Regenerative Medicine,Institute for Translational Medicine,College of Medicine,Qingdao University,Qingdao 266000,Shandong,P.R.China [3]Department of Thoracic Surgery,Affiliated Hospital of Qingdao University,Qingdao 266000,Shandong,P.R.China [4]Department of Gastroenterology,The Seventh Medical Center of PLA General Hospital,Beijing 100700,China

出　　处：《Cancer Communications》2019年第1期655-664,共10页癌症通讯（英文）

基　　金：This work was supported by the National Natural Science Foundation of China(81622005);Beijing Natural Science Foundation(7172213).

摘　　要：Clinical practice has shown that Parkin is the major causative gene found in an autosomal recessive juvenile parkin-sonism(AR-JP)via Parkin mutations and that the Parkin protein is the core expression product of the Parkin gene,which itself belongs to an E3 ubiquitin ligase.Since the discovery of the Parkin gene in the late 1990s,researchers in many countries have begun extensive research on this gene and found that in addition to AR-JP,the Parkin gene is associated with many diseases,including type 2 diabetes,leprosy,Alzheimer’s,autism,and cancer.Recent studies have found that the loss or dysfunction of Parkin has a certain relationship with tumorigenesis.In general,the Parkin gene,a well-established tumor suppressor,is deficient and mutated in a variety of malignancies.Parkin overexpres-sion inhibits tumor cell growth and promotes apoptosis.However,the functions of Parkin in tumorigenesis and its regulatory mechanisms are still not fully understood.This article describes the structure,functions,and post-transla-tional modifications of Parkin,and summarizes the recent advances in the tumor suppressive function of Parkin and its underlying mechanisms.

关 键 词：PARKIN E3 ubiquitin ligase CANCER Post-translational modification Parkin/PTEN-induced kinase 1(PINK1) NIP3-like protein X UBIQUITINATION SUMOYLATION NEDDYLATION Phosphorylation 

分 类 号：R74[医药卫生—神经病学与精神病学]