Regulation of Fanconi anemia protein FANCD2 monoubiquitination by miR-302
| Autor: | Suresh Ramakrishna, Hoe Su Jeong, A. Madhan Kumar, Kye Seong Kim, Bharathi Suresh, Youl Hee Cho |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
congenital
hereditary and neonatal diseases and abnormalities DNA repair Biophysics Regulator Biology Biochemistry Ubiquitin Fanconi anemia Cell Line Tumor hemic and lymphatic diseases FANCD2 microRNA medicine Humans Monoubiquitination Molecular Biology Fanconi Anemia Complementation Group D2 Protein Ubiquitination Bone marrow failure nutritional and metabolic diseases Cell Biology medicine.disease Molecular biology Cell biology MicroRNAs biology.protein |
| Zdroj: | Biochemical and Biophysical Research Communications. 466:180-185 |
| ISSN: | 0006-291X |
| Popis: | Fanconi anemia (FA) is a recessively inherited multigene disease characterized by congenital defects, progressive bone marrow failure, and heightened cancer susceptibility. Monoubiquitination of the FA pathway member FANCD2 contributes to the repair of replication stalling DNA lesions. However, cellular regulation of FANCD2 monoubiquitination remains poorly understood. In the present study, we identified the miR-302 cluster as a potential regulator of FANCD2 by bioinformatics analysis. MicroRNAs (miRNAs) are the major posttranscriptional regulators of a wide variety of biological processes, and have been implicated in a number of diseases. Expression of the exogenous miR-302 cluster (without miR-367) reduced FANCD2 monoubiquitination and nuclear foci formation. Furthermore, miR-302 cells showed extensive chromosomal breakage upon MMC treatment when compared to mock control cells. Taken together, our results suggest that overexpression of miR-302 plays a critical role in the regulation of FANCD2 monoubiquitination, resulting in characteristic defects in DNA repair within cells. |
| Databáze: | OpenAIRE |
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