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. 2013 Feb 1;24(3):351–360. doi: 10.1091/mbc.E12-07-0561

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© 2013 Estarás et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 4: — JMJD3 is essential for RNAPII elongation. (A) Relative mRNA levels of neurogenin 2 in C KD and JMJD3 KD NSCs untreated or treated with TGFβ for the times indicated in the legend. (B, C) ChIP assays analyzed by qPCR performed in C KD and JMJD3 KD NSC lines before (0 h) and after (0.5 and 3 h) TGFβ treatment using total RNAPII (N20; B) or RNAPII-S2p (ab5095; C) antibodies. Analyzed gene regions are indicated in the corresponding scheme. Normalized basal conditions and fold recruitment upon TGFβ treatment in C KD and JMJD3 KD cell lines are represented. (D) Summary of the results. In TGFβ-stimulated C KD cells the transcription machinery is uploaded to the promoters and spreads within the body of genes to generate new mRNA. In TGFβ-stimulated JMJD3 KD cells, the recruitment of RNAPII to promoters occurs to the same extent as in control cells, but the RNAPII progression along the gene bodies is impaired.