Inhibition of USP14 and UCH37 deubiquitinating activity by b-AP15 as a potential therapy for tumors with p53 deficiency
作者机构：Central Laboratory for Medical ResearchShanghai Tenth People’s HospitalTongji University School of Medicine200072 ShanghaiChina Cancer InstituteNantong Tumor Hospital226631 NantongChina Department of Nuclear MedicineShanghai Tenth People’s HospitalTongji University School of Medicine200072 ShanghaiChina Department of RadiologyThe Fourth Affiliated Hospital of Anhui Medical University230012 HefeiChina Department of OrthopedicsZhongshan HospitalFudan University200032 ShanghaiChina Department of Hand SurgeryShenzhen Longhua District People’s Hospital518109 ShenzhenChina National Engineering Laboratory for Rice and By-product Deep ProcessingCollege of Food Science and EngineeringCentral South University of Forestry and Technology410004 ChangshaChina
出 版 物：《Signal Transduction and Targeted Therapy》 (信号转导与靶向治疗（英文）)
年 卷 期：2020年第5卷第1期
页 面：2100-2102页
核心收录：
学科分类：0710[理学-生物学] 1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
基 金：supported partly by grants from the National Natural Science Foundation of China Scientific Research Fund Project of Anhui Medical University Construction of Clinical Medical Center for Tumor Biological Samples in Nantong Jiangsu 333 Program
摘 要：Dear Editor,Tumor-suppressor protein p53 is important for cell function and genome integrity.1 The decrease of p53 protein is a common feature of human malignant tumors,which leads to the deficiency of cell cycle detection point control and apoptosis *** enormous amount of research effort goes into small molecules that regulate p53,including wild-type repair of mutant p53 gene and interruption of the binding between p53 and an E3-ubiquitin ligase Mdm2 to prevent ubiquitination degradation of p53 and rescue the protein level of p53.2 However,it is not clear whether it is necessary to continue to inhibit the ubiquitin activity of proteasome in order to restore the p53 protein level.
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