Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김계성 | - |
dc.date.accessioned | 2017-08-01T05:20:25Z | - |
dc.date.available | 2017-08-01T05:20:25Z | - |
dc.date.issued | 2015-10 | - |
dc.identifier.citation | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v. 466, NO 2, Page. 180-185 | en_US |
dc.identifier.issn | 0006-291X | - |
dc.identifier.issn | 1090-2104 | - |
dc.identifier.uri | http://www.sciencedirect.com/science/article/pii/S0006291X15305179?via%3Dihub | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/28160 | - |
dc.description.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. | en_US |
dc.description.sponsorship | We thank Prof. Hal E. Broxmeyer for providing the miR-302 (b/c/a/d) lentiviral construct and Prof. Chang Hwan Park for providing the EGFP-IRES3-CHE5 lentiviral vector. We also thank Patty Mantel for revising and editing our manuscript and Kim Su-Jin for her technical assistance. This study was supported by a grant from the Korea Health Technology Research and Development project, Ministry of Health and Welfare, Republic of Korea (A120262). | en_US |
dc.language.iso | en | en_US |
dc.publisher | ACADEMIC PRESS INC ELSEVIER SCIENCE | en_US |
dc.subject | Chromosomal breakage | en_US |
dc.subject | DNA repair | en_US |
dc.subject | Fanconi anemia pathway | en_US |
dc.subject | Monoubiquitination | en_US |
dc.subject | Nuclear foci | en_US |
dc.title | Regulation of Fanconi anemia protein FANCD2 monoubiquitination by miR-302 | en_US |
dc.type | Article | en_US |
dc.relation.no | 2 | - |
dc.relation.volume | 466 | - |
dc.identifier.doi | 10.1016/j.bbrc.2015.08.127 | - |
dc.relation.page | 180-185 | - |
dc.relation.journal | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.contributor.googleauthor | Suresh, Bharathi | - |
dc.contributor.googleauthor | Kumar, A. Madhan | - |
dc.contributor.googleauthor | Jeong, Hoe-Su | - |
dc.contributor.googleauthor | Cho, Youl-Hee | - |
dc.contributor.googleauthor | Ramakrishna, Suresh | - |
dc.contributor.googleauthor | Kim, Kye-Seong | - |
dc.relation.code | 2015001367 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | ks66kim | - |
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