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. 2016 Dec 2;6:38421. doi: 10.1038/srep38421

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Copyright © 2016, The Author(s)

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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TM expression is increased soon after PMA induction in THP-1 cells. TM may regulate PMA-induced THP-1 cell differentiation via a direct interaction with PKCδ. TM acts as a scaffold for PKCδ docking, which keeps PKCδ in the region close to the membrane and promotes subsequent ERK1/2 activation. ERK1/2 activation subsequently enhances the expression of cell cycle inhibitor p21^Cip1/WAF1 via NF-kB p65 signaling, which causes cell cycle arrest and promotes differentiation. On the other hand, ERK1/2 activation participates in the phosphorylation of paxillin, cofilin, LIMK1, and PYK2, which interact with TM and mediate cytoskeleton remodeling to promote differentiation.