Fig 1: PCA negatively regulates the osteoclastogenesis-associated MAPK and Akt signaling pathways and critical nuclear factors. RAW 264.7 cells were treated with PCA for 2 h and cultured with RANKL for the corresponding time. (A) Western blotting was used to analyze the total protein extracts of proteins associated with the MAPKs and Akt signaling pathways. Phosphorylation of MAPKs (ERK, p-38 and JNK) and Akt was quantified. (B) Western blotting was used to analyze the expression of p65, c-Fos and NFATc1. All data represent at least three independent experiments. Values represent the mean ± SEM. **P<0.01 vs. sham; #P<0.05, ##P<0.01 vs. RANKL. MAPK, mitogen-activated protein kinases; NFATc1, nuclear factor of activated T cells 1; p, phosphorylated; PCA, protocatechuic acid; RANKL, receptor activator of nuclear factor-κB ligand.
Fig 2: FGF22-induced calcium influx activates CalN to inhibit MEF2D in mouse hair cells. (A, B) CalN levels in transduced hair cells by RT-qPCR (A), and by ELISA (B). (C) NFATc levels in transduced hair cells by RT-qPCR. (D, E) Cultured hair cells were transduced with AAV-CalN or AAV-shCalN or control AAV-scr (scramble) and assessed for MEF2D levels by RT-qPCR (D), and by ELISA (E). *p<0.05. NS: non-significant. N=5.
Fig 3: Schematic of the model. Regulation of ribbon synapses by FGF22/calcium/CalN/MEF2D signaling. FGF22 signaling through its major receptor FGFE2b triggers an increase of intracellular Ca2+, which activates the CaN and its downstream factors, e.g. NFATc. Activated CaN subsequently suppresses MEF2D, the inhibitory effects of which on ribbon synapses are then released.
Supplier Page from Abcam for NFATc1 Transcription Factor Assay Kit (Colorimetric)