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Volume 29, No 8, Aug 2019

ISSN: 1001-0602 
EISSN: 1748-7838 2018 
impact factor 17.848* 
(Clarivate Analytics, 2019)

Volume 29 Issue 8, August 2019: 683-685

LETTERS TO THE EDITOR

Structural insights into the activation of ATM kinase

Jianxiong Xiao 1,2, Mengjie Liu 1,2, Yilun Qi1, Yuriy Chaban3,Chao Gao1, Beiqing Pan1, Yuan Tian1, Zishuo Yu1, Jie Li4,Peijun Zhang 3,5 and Yanhui Xu 1,2,6,7

1 Fudan University Shanghai Cancer Center, Institutes of Biomedical Sciences, State Key Laboratory of Genetic Engineering and Key Laboratory of Medical Epigenetics and Metabolism, Shanghai Medical College of Fudan University, Shanghai 200032, China; 2Key Laboratory of Molecular Medicine, Ministry of Education, Department of Systems Biology for Medicine, School of Basic Medical Sciences, Shanghai Medical College of Fudan University, Shanghai 200032,China; 3Electron Bio-Imaging Centre, Diamond Light Sources, Harwell Science and Innovation Campus, Didcot, Oxfordshire, UK; 4National Facility for Protein Science in Shanghai, Zhangjiang Lab, Shanghai 201210, China; 5Division of Structural Biology, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK; 6Collaborative Innovation Center of Genetics and Development, School of Life Sciences, Fudan University, Shanghai 200433, China and 7CAS Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai 200031, China
These authors contributed equally: Jianxiong Xiao, Mengjie Liu, Yilun Qi, Yuriy Chaban, Chao Gao. Correspondence: Yanhui Xu (xuyh@fudan.edu.cn)

Dear Editor,

ATM (ataxia telangiectasia-mutated) is a master regulator in response to DNA damage and activates downstream pathways involved in cell cycle checkpoints, DNA damage repair, transcription regulation, immune response, central nervous system development and metabolism.1,2 Loss of ATM activity in human results in the pleiotropic neurodegeneration disorder ataxia-telangiectasia (A-T) that is characterized by immunodeficiency, cancer predisposition, premature aging and insulin-resistant diabetes.3,4,5 Despite extensive studies over the past two decades,6,7 it remains controversial how ATM is activated. Particularly, whether ATM exists in a monomeric form, whether the monomer is more active than dimer, and how dimer-to-monomer transition affects the ATM kinase activity, remain controversial.


https://doi.org/10.1038/s41422-019-0205-0

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