Regulation of Tumor Suppressor Gene CDKN2A and Encoded p16-INK4a Protein by Covalent Modifications
- 作者: Jiao Y.1, Feng Y.2, Wang X.3
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隶属关系:
- School of Physical Education
- Key Laboratory of Molecular Epigenetics, Ministry of Education
- Central Laboratory of General Biology, School of Life Sciences
- 期: 卷 83, 编号 11 (2018)
- 页面: 1289-1298
- 栏目: Review
- URL: https://journals.rcsi.science/0006-2979/article/view/151748
- DOI: https://doi.org/10.1134/S0006297918110019
- ID: 151748
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详细
CDKN2A is one of the most studied tumor suppressor genes. It encodes the p16-INK4a protein that plays a critical role in the cell cycle progression, differentiation, senescence, and apoptosis. Mutations in CDKN2A or dysregulation of its functional activity are frequently associated with various types of human cancer. As a cyclin-dependent kinase inhibitor, p16-INK4a forms a complex with cyclin-dependent kinases 4/6 (CDK4/6) thereby competing with cyclin D. It is believed that the helix-turn-helix structures in the content of tandem ankyrin repeats in p16-INK4a are required for the protein interaction with CDK4. Until recently, the mechanisms considered to be involved in the regulation of p16-INK4a functions and cancer development have been mutations in DNA, homozygous or heterozygous gene loss, and methylation of CDKN2A promoter region. In this review, we discuss recent findings on the regulation of p16-INK4a by covalent modifications at both transcriptional and post-translational levels.
作者简介
Yang Jiao
School of Physical Education
Email: wangxl034@nenu.edu.cn
中国, Changchun, Jilin, 130024
Yunpeng Feng
Key Laboratory of Molecular Epigenetics, Ministry of Education
Email: wangxl034@nenu.edu.cn
中国, Changchun, Jilin, 130024
Xiuli Wang
Central Laboratory of General Biology, School of Life Sciences
编辑信件的主要联系方式.
Email: wangxl034@nenu.edu.cn
中国, Changchun, Jilin, 130024
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