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. 2019 Jan 23;8(2):bio039800. doi: 10.1242/bio.039800

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© 2019. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Fig. 2. — αSMA-CreER effectively deletes Foxf1 from hepatic myofibroblasts. (A,B) FOXF1 co-localizes with DES in HSCs before and after CCl₄-induced injury. FOXF1 co-localizes with DES and αSMA in MFs after chronic liver injury. αSMA-CreER effectively deletes Foxf1 from MFs after Tam treatment. (C) Western blot shows total liver protein levels of FOXF1 are decreased in αSMACreER;Foxf1^−/− livers after CCl₄ injury. Cropped blots are presented here with full length blots presented in Fig. S12. (D) Quantification of western blot revealed a significant loss of FOXF1 in αSMACreER;Foxf1^−/− livers. Quantification was averaged across four blots. FOXF1 levels were internally normalized to ACTIN for each sample. *P<0.05. (E) FOXF1 staining is detected in liver parenchyma and fibrotic regions (yellow arrows). FOXF1 staining is decreased in fibrotic regions of αSMACreER;Foxf1^−/− livers (white arrows).