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. 2017 Apr 13;7:877. doi: 10.1038/s41598-017-00707-6

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© The Author(s) 2017

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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Activity-dependent regulation of FOXP1 SUMOylation. (A) Cultured cortical neurons (DIV7) were depolarised for 30 min with KCl in ACSF, lysed in sample buffer and resolved by SDS-PAGE followed by immunoblotting with the indicated antibodies. Student’s t-test, n = 4, **p < 0.01. (B) Cortical neurons were treated with the indicated drugs, lysed in sample buffer and samples resolved by SDS-PAGE and immunoblotting. NMDA receptor activation decreases FOXP1 SUMOylation. Note the lower exposure in the middle panel indicates unchanged expression levels of unmodified FOXP1. Student’s t-test and Welch correction, n = 5 **p < 0.001. (C) Calcium entry through NMDARs and L-type calcium channels reduces FOXP1 SUMOylation. Cultures were pre-treated with the NMDAR antagonist AP5, the L-type calcium channel blocker nimodipine or EGTA to chelate extracellular Ca²⁺ prior to glutamate stimulation. Data normalised to no glutamate, DMSO control. ANOVA, n = 5, **p < 0.01, *p < 0.05.