Regulation of Tumor Suppressor Gene CDKN2A and Encoded p16-INK4a Protein by Covalent Modifications
| Autor: | Yunpeng Feng, Yang Jiao, Xiuli Wang |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Tumor suppressor gene Biology medicine.disease_cause Biochemistry 03 medical and health sciences 0302 clinical medicine CDKN2A Neoplasms medicine Animals Cyclin-Dependent Kinase Inhibitor p18 Humans neoplasms Gene Cyclin-Dependent Kinase Inhibitor p16 Mutation integumentary system Kinase Cyclin-Dependent Kinase 4 Cyclin-Dependent Kinase 6 DNA Neoplasm General Medicine DNA Methylation Cell cycle Cell biology 030104 developmental biology 030220 oncology & carcinogenesis DNA methylation Ankyrin repeat biological phenomena cell phenomena and immunity Protein Processing Post-Translational |
| Zdroj: | Biochemistry (Moscow). 83:1289-1298 |
| ISSN: | 1608-3040 0006-2979 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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