Regulation of Fanconi anemia protein FANCD2 monoubiquitination by miR-302

Title
Regulation of Fanconi anemia protein FANCD2 monoubiquitination by miR-302
Author
Ramakrishna, Suresh
Keywords
Chromosomal breakage; DNA repair; Fanconi anemia pathway; Monoubiquitination; Nuclear foci
Issue Date
2015-10
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v. 466, NO 2, Page. 180-185
Abstract
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. (C) 2015 Elsevier Inc. All rights reserved.
URI
http://www.sciencedirect.com/science/article/pii/S0006291X15305179?via%3Dihubhttp://hdl.handle.net/20.500.11754/28164
ISSN
0006-291X; 1090-2104
DOI
10.1016/j.bbrc.2015.08.127
Appears in Collections:
GRADUATE SCHOOL OF BIOMEDICAL SCIENCE AND ENGINEERING[S](의생명공학전문대학원) > ETC
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