Lamin A buffers CK2 kinase activity to modulate aging in a progeria mouse model.

Author:

Ao Ying12,Zhang Jie1,Liu Zuojun1,Qian Minxian1,Li Yao3,Wu Zhuping1,Sun Pengfei1,Wu Jie1,Bei Weixin1,Wen Junqu1,Wu Xuli3,Li Feng2,Zhou Zhongjun4ORCID,Zhu Wei-Guo1ORCID,Liu Baohua1ORCID,Wang Zimei1ORCID

Affiliation:

1. Guangdong Key Laboratory of Genome Stability and Human Disease Prevention, Carson International Cancer Center, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Health Science Center, Shenzhen 518060, China.

2. Department of Genetics, School of Basic Medical Sciences, Wuhan University, Wuhan 430071, Hubei, China.

3. School of Public Health, Shenzhen University Health Science Center, Shenzhen 518060, China.

4. School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, 21 Sassoon Road, Hong Kong.

Abstract

The causative progeria lamin A mutation inhibits CK2 enzyme activity to accelerate aging in laboratory mice.

Funder

National Natural Science Foundation of China

Discipline Construction Funding of Shenzhen

Shenzhen Municipal Commission of Science and Technology Innovation

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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