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. 2015 Mar 26;43(9):4505–4516. doi: 10.1093/nar/gkv176

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© The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 6. — Schematic of AKT1-mediated H3-T45 phosphorylation in transcriptional termination on DNA damage. DNA damage triggers the transcription of stress-response genes by RNA Pol II. As transcription progresses through the 3′ region of the locus, RNA Pol II-S2 undergoes hyperphosphorylation and DNA damage-activated AKT1 phosphorylates H3-T45. When RNA Pol II passes through the 3′ area of the poly(A) site, pre-mRNA is cleaved and is processed into mature mRNA (12,14). Phosphorylated H3-T45 accelerates the degradation of 5′ unprotected RNA downstream of the poly(A) site to induce the dissociation of RNA Pol II from chromatin.