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Description Figure 7. The suggested new signaling pathways induced by Noggin in human ASC osteogenic cultures. We have demonstrated that Noggin can activate FGFR2 receptors and Src kinase associated with the receptor complex. This results in ERK1/2 phosphorylation and, independently of PI3k, Akt kinase phosphorylation. It is known that dexamethasone, a component of osteogenic medium, stimulates RUNX2 and TAZ expressions. We have shown Noggin activation of Akt that leads to blocking the ability of GSK3 to degrade TAZ and suppress RUNX2 activity, thereby stabilizing TAZ and enhancing formation of RUNX2-TAZ complexes. Whereas RUNX2-TAZ complexes can be phosphorylated by Noggin-activated ERK1/2. Such activated RUNX2-TAZ complexes are required for the transcription of osteogenic genes. Besides, we have shown Noggin-related inhibition of SMAD1/5/8 activity, which may be a result of increased SMAD 7 expression due to Akt activity. Figure was created in Affinity Designer software (1.10.6).
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Source https://www.nature.com/articles/s41598-024-56858-w Truchan, K., Osyczka, A.M. Noggin promotes osteogenesis in human adipose-derived mesenchymal stem cells via FGFR2/Src/Akt and ERK signaling pathway. Sci Rep 14, 6724 (2024). https://doi.org/10.1038/s41598-024-56858-w
Author Truchan, K., Osyczka, A.M.
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current22:17, 15 December 2024Thumbnail for version as of 22:17, 15 December 20241,699 × 913 (688 KB)Rasbak (talk | contribs){{Information |Description=Figure 7. The suggested new signaling pathways induced by Noggin in human ASC osteogenic cultures. We have demonstrated that Noggin can activate FGFR2 receptors and Src kinase associated with the receptor complex. This results in ERK1/2 phosphorylation and, independently of PI3k, Akt kinase phosphorylation. It is known that dexamethasone, a component of osteogenic medium, stimulates RUNX2 and TAZ expressions. We have shown Noggin activation of Akt that leads to bloc...

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