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. 2019 Apr 29;10:278. doi: 10.3389/fpsyt.2019.00278

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Copyright © 2019 Sanfeliu, Hokamp, Gill and Tropea

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Proposed mechanism linking Mecp2, Ube2v1, and Rett syndrome (RTT). (A) In neurons, MeCP2 would upregulate the transcription of Ube2v1, directly or indirectly. UBE2V1, together with UBC13 and TRAF6, would promote Lys63-linked ubiquitination of PSD95, which would in turn regulate AMPA receptor (AMPAR) trafficking. (B) In peripheral blood mononuclear cells (PBMCs), MeCP2 would repress the transcription of Ube2v1 (directly or not). UBE2V1, together with UBC13 and TRAF6, would activate IκB kinase (IKK), which would activate the NFκB pathway. This would promote the transcription of proinflammatory genes and the upregulation of cytokines such as TNFα, IL-6, and IL-3.