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. 2014 Nov 26;1(1):e970883. doi: 10.4161/23262125.2014.970883

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© 2014 The Author(s). Published with license by Taylor & Francis Group, LLC

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

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Figure 8. — Schematic model depicting the proposed role of CREB in the proliferation of embryonic neural progenitors. (A) Under normal conditions phosphorylated CREB (pCREB) binds to cAMP-responsive element (CRE) and recruits CBP promoting histone acetylation (Ac) of targets genes which in turn lead to clone formation. (B) Upon CREB ablation, CBP is not capable of maintaining histone acetylation and clonogenic activity of neural progenitors is impaired. (C) Treatment with the histone deacetylase inhibitor TSA prevents the loss of histone acetylation and rescues the deficit in clone formation observed in the absence of CREB suggesting that CREB regulates proliferation essentially by modification of chromatin structure.