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. 2017 May 30;25(4):354–361. doi: 10.4062/biomolther.2016.263

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Copyright ©2017, The Korean Society of Applied Pharmacology

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.

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Fig. 2. — Role of TAZ in LPA-induced migration and proliferation of MEFs. (A) Wild-type MEFs (control) and TAZ-knockout MEFs (TAZ-KO) were treated with the various concentrations of LPA for 12 h, followed by a chemotactic migration assay. Data indicate mean ± SD. ^*p<0.05 (n=8). (B) Inhibition of LPA-induced proliferation in the TAZ-knockout MEFs is shown. Wild-type MEFs (control) and TAZ-knockout MEFs (TAZ-KO) were treated with vehicles or LPA (10 μM) for 3 days. The number of cells were counted and compared with those of the control cells. TAZ-knockout MEFs exhibited decreased LPA-induced proliferation for 3 days. The cellular proliferation rate was determined via cell counting using trypan blue inclusion assay. Data indicate mean ± SD. ^*p<0.05 (n=6). (C) Time-course of LPA-induced TAZ expression is shown. Wild-type MEFs (control) and TAZ-knockout MEFs (TAZ-KO) were treated with vehicle or LPA (10 μM) for the indicated periods. The expression levels of TAZ and GAPDH were determined using Western blotting.