Abrogation of nuclear entry of TERT by fructose 1,6-bisphosphatase 1-mediated dephosphorylation  

作　　者：Pengbo Yao Gaoxiang Zhao Min Li Wensheng Qiu Zhimin Lu 

机构地区：[1]Department of Oncology,The Affiliated Hospital of Qingdao University,Qingdao University,Qingdao Cancer Institute,Qingdao,Shandong,P.R.China [2]Zhejiang Provincial Key Laboratory of Pancreatic Disease,The First Affiliated Hospital,and Institute of Translational Medicine,Zhejiang University School of Medicine,Hangzhou,Zhejiang,P.R.China [3]Cancer Center,Zhejiang University,Hangzhou,Zhejiang,P.R.China [4]Institute of Fundamental and Transdisciplinary Research,Zhejiang University,Hangzhou,Zhejiang,P.R.China

出　　处：《Cancer Communications》2024年第10期1102-1105,共4页癌症通讯（英文）

基　　金：the Ministry of Science and Technology of the People’s Republic of China,Grant/Award Number:2020YFA0803300;National Center of Technology Innovation for Biopharmaceuticals,Grant/Award Number:NCTIB2022HS02006;Taishan Scholar Project from Shandong province,Grant/Award Number:tsqn202312174;National Natural Science Foundation of China,Grant/Award Numbers:82030074,82103351,82188102。

摘　　要：Telomeres maintain chromosome integrity.Loss of telomere function,which is attributed to progressively shortened telomeres in each round of DNA replication,induces endto-end fusion of chromosomes,anaphase bridges with subsequent chromosome breakage,and eventually leads to senescence and apoptosis in normal cells[1].In cancer cells,highly activated telomerase synthesizes telomere repeats to promote telomere elongation.

关 键 词：eventually BRIDGES MAINTAIN 

分 类 号：R73[医药卫生—肿瘤]