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. 2020 Jun 9;21(11):4104. doi: 10.3390/ijms21114104

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Schematic illustration of the suggested mechanism of Pref-1-mediated inhibition of adipogenesis involving the MEK/ERK pathway. (1) TACE-mediated cleavage of membrane bound Pref-1. (2) 50 kDA soluble Pref-1 binds to the C-terminus of fibronectin. (3) Fibronectin binds to the α5β1 integrin receptor and the fibronectin/sPref-1 complex (4) activates the MEK/ERK pathway, which in turn (5) activates SOX9. (6) SOX9 binds to the C/EBPβ promoter, preventing up-regulation of C/EBPβ and (7) consequently up-regulation of C/EBPα and PPARγ. Figure adapted by C.D. from Hudak and Sul (2013) [100]. C/EBPα, CAAT-enhancer binding protein alpha; C/EBPβ, CAAT-enhancer binding protein beta; ERK, Extracellular signal-regulated kinases; MEK, Mitogen-activated protein kinase kinase; mPref-1, membrane-bound preadipocyte factor-1; sPref-1, soluble preadipocyte factor-1; PPARγ, Peroxisome proliferator-activated receptor gamma; TACE, Tumor necrosis factor alpha converting enzyme.