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. 2018 Jan 26;8:1678. doi: 10.1038/s41598-018-19806-z

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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SAM68 modulates the biogenesis of miR-29s at the transcriptional level. (a) Level of precursor and mature miR-29a, b and c in N2a cells after Sam68 knockdown. **p < 0.01, ***p < 0.001 determined by unpaired t test (b) Level of precursor and mature miR-29a, b and c in N2a cells after Sam68 overexpression. *p < 0.05 determined by unpaired t test. (c) Level of Tet1, 2 and 3 after overexpression of Sam68 or control measured by RT-qPCR. ***p < 0.001 determined by unpaired t test. (d) Level of nuclear pri-miR29a/b-1, pre-miR-29a, pre-miR-29b and pre-miR-29c transcripts in N2a cells after Sam68 knockdown measured by RT-qPCR in the presence of ActD treatment or vehicle. **p < 0.01, ***p < 0.001 determined by two-way ANOVA followed by Bonferroni’s post-hoc test. Data represent mean ± s.e.m.