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The mitogen-activated protein kinase (MAPK) family members, extracellular signaling-regulated kinase (ERK) and p38 are required in the mitotic clonal expansion (MCE) stage of adipogenesis to facilitate the phosphorylation of CCAAT/enhancer-binding protein β (C/EBPβ), as well as to facilitate a G9a-mediated time lag between this phosphorylation and the expression of peroxisome proliferator-activated receptor γ (PPARγ) and C/EBPα. It has also been shown that the MAPK c-Jun amino-terminal kinase (JNK) plays a role in lineage commitment, and its activation will determine if mesenchymal stem cells will differentiate into osteoblasts or adipo
blasts. It is clear that tight regulation of the different MAPK cascades is required for proper adipocyte differentiation. Furthermore, other pathways and a chorus of other factors are also necessary for MCE to proceed, such as the ability of Akt to activate mechanistic target of rapamycin complex 1 (mTORC1) and its downstream effector eIF4E, which are required for S-phase kinase-associated protein 2 (Skp2) mRNA translation, which then degrades p21 and p27 proteins. Expression of the fat mass and obesity-associated gene (FTO) and factor for adipocyte differentiation (FAD) gene are also necessary for MCE. The interplay of these elements illustrates the necessity of MAPKs and other molecular actors in the crucial adipogenic step of MCE.