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. 2015 Jun 16;16:34. doi: 10.1186/s12868-015-0171-5

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© Dickson et al. 2015

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Inhibition of the Shroom3–ROCK protein–protein interaction with CCG-17444 enhances neurite outgrowth. P19-derived neurons were treated with 25 μM CCG-17444 or vehicle control (DMSO) for 24 h. a, b CCG-17444 enhances neurite length in neurons transfected with an RNAi control vector. Neurons transfected with POSH RNAi or Shroom3 RNAi vectors exhibit enhanced neurite length due to reduction of POSH or Shroom3 function but CCG-17444 does not further enhance neurite length, suggesting that CCG-17444 selectively targets the POSH/Shroom3 signaling complex (n = 3). Student’s t test: *p < 0.0001, Control RNAi vs CCG-17444 treated Control RNAi; ^#p < 0.0001, Control RNAi vs Shroom3 or POSH RNAi; **p < 0.0005, CCG-17444 Control RNAi vs CCG-17444 Shroom3 RNAi; ⁺p < 0.0001, CCG-17444 Control RNAi vs CCG-17444 POSH RNAi. Scale bar 100 μm.