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nArgBP2 as a hub molecule in the etiology of various neuropsychiatric disorders
nArgBP2 as a hub molecule in the etiology of various neuropsychiatric disorders
BMB Reports. 2016. Sep, 49(9): 457-458
Copyright © 2016, Korean Society for Biochemistry and Molecular Biology
This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
  • Received : August 09, 2016
  • Published : September 30, 2016
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Sang-Eun Lee
Sunghoe Chang
sunghoe@snu.ac.kr

Abstract
Recent studies have strongly implicated postsynaptic scaffolding proteins such as SAPAP3 or Shank3 in the pathogenesis of various mood disorders, including autism spectrum disorder, bipolar disorder (BD), and obsessive-compulsive disorders. Neural Abelson-related gene-binding protein 2 (nArgBP2) was originally identified as a protein that interacts with SAPAP3 and Shank3. Recent study shows that the genetic deletion of nArgBP2 in mice leads to manic/bipolar-like behavior resembling symptoms of BD. However, the function of nArgBP2 at synapse, or its connection with the synaptic dysfunctions, is completely unknown. This study provides compelling evidence that nArgBP2 regulates the spine morphogenesis through the activation of Rac1/WAVE/PAK/cofilin pathway, and that its ablation causes a robust and selective inhibition of excitatory synapse formation, by controlling actin dynamics. Our results revealed the underlying mechanism for the synaptic dysfunction caused by nArgBP2 downregulation that associates with analogous human BD. Moreover, since nArgBP2 interacts with key proteins involved in various neuropsychiatric disorders, our finding implies that nArgBP2 could function as a hub linking various etiological factors of different mood disorders. [BMB Reports 2016; 49(9): 457-458]
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Acknowledgements
This research was supported by Grant NRF-2015M3C7A10 28790 from the Brain Research Program through the National Research Foundation of Korea, and Grant 20100029395 from the Biomembrane Plasticity Research Center funded by the Ministry of Science, ICT & Future Planning, Republic of Korea.
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