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Biomolecules 2015, 5(3), 1600-1617;

Transcription Blockage Leads to New Beginnings

Department of Radiation Oncology and Translational Oncology Program, University of Michigan Medical School, Ann Arbor, MI 48109, USA
Department of Microbiology, Biomedical Sciences Institute, University of São Paulo, São Paulo 05508-000, Brazil
Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, MI 48109, USA
Novartis Institutes of Biomedical Sciences, Cambridge, MA 02139, USA
Department of Environmental Health Sciences, University of Michigan, Ann Arbor, MI 48109, USA
Author to whom correspondence should be addressed.
Academic Editors: Wolf-Dietrich Heyer, Thomas Helleday and Fumio Hanaoka
Received: 23 June 2015 / Revised: 9 July 2015 / Accepted: 16 July 2015 / Published: 21 July 2015
(This article belongs to the Special Issue DNA Damage Response)
Full-Text   |   PDF [2071 KB, uploaded 21 July 2015]   |  


Environmental agents are constantly challenging cells by damaging DNA, leading to the blockage of transcription elongation. How do cells deal with transcription-blockage and how is transcription restarted after the blocking lesions are removed? Here we review the processes responsible for the removal of transcription-blocking lesions, as well as mechanisms of transcription restart. We also discuss recent data suggesting that blocked RNA polymerases may not resume transcription from the site of the lesion following its removal but, rather, are forced to start over from the beginning of genes. View Full-Text
Keywords: DNA damage; DNA repair; RNA polymerase II; recovery of RNA synthesis DNA damage; DNA repair; RNA polymerase II; recovery of RNA synthesis

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

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Andrade-Lima, L.C.; Veloso, A.; Ljungman, M. Transcription Blockage Leads to New Beginnings. Biomolecules 2015, 5, 1600-1617.

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