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. 2017 May 4;12:34. doi: 10.1186/s13024-017-0178-8

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© The Author(s). 2017

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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Fig. 8 — The proposed working model by which ANP32A regulates synaptic plasticity and cognitive function. The neurotoxic insults, such as htau accumulation, or Aβ-fibrils or H₂O₂ overproduction, activate C/EBPβ by increasing its protein level and promoting its phosphorylation at Thr238/188. The activated C/EBPβ binds to its responsive element (CCAAT box) in the proximal ANP32A promoter region, and thus stimulates the expression of ANP32A. Then ANP32A interacts with SET to form INHAT, which masks histones for acetylation by HAT. Hypo-acetylation of histone inhibits transcription of synapse-associated proteins, leading to cognitive deficits. Arresting ANP32A overproduction unmasks histone for a robust acetylation, and thus increases the transcription of synaptic plasticity-related proteins to preserve learning and memory capacities