2015年11月30日 · Here we identify the transcription factor NFATc4 as a functional link connecting inflammation-induced EGFR signaling to acinar metaplasia and show that induction of Sox9 in response to EGFR activation requires NFATc4-dependent transcriptional activation of …

Our findings identify an EGFR-NFATc1-Sox9 signaling cascade as a critical mediator of inflammation-induced PDAC initiation and suggest that disruption of this pathway may offer a novel chemopreventive target for high-risk pancreatitis patients. Keywords: signal transduction, mouse model, transcriptional regulation, ChIP, NFATc1, EGFR.

2014年5月13日 · Mechanistically, Ca (2+) influx via Cav3.2 activates the calcineurin/nuclear factor of the activated T-cell (NFAT) signaling pathway, and a previously unidentified NFAT binding site is identified within the mouse Sox9 promoter using a …

We identified an NFAT binding motif (TTTCC) in the mouse Sox9 promoter that was required for Ca v 3.2-dependent Sox9 regulation on Luc reporter assay. In addition, NFAT directly bound to the identified sequence on gel shift, supershift, and ChIP assays.

2021年1月1日 · Sox9 in situ hybridization after 24 h of WNT5A or CaN inhibitor or NFAT inhibitor bead implantation followed by 1 h or 4 h of TGFβ treatment. Experimental design showing initial WNT5A, CaN or NFAT inhibitors or control vehicle bead implantation (time 0) in the interdigit.

Mechanistically, Wnt5a acts to increase chondrocyte differentiation at an early stage through calmodulin kinase /NFAT-dependent induction of Sox9. Conversely, Wnt5a represses chondrocyte hypertrophy via NF-κB-dependent inhibition of Runx2 expression.

2015年5月1日 · Induction of EGFR signaling and its effects on the expression of Nuclear factor of activated T cells c1 (NFATc1) or SOX9 were investigated by quantitative reverse-transcription polymerase chain reaction, immunoblot, and immunohistochemical analyses of mouse and human tissues and acinar cell explants.

Induction of EGFR signaling and its effects on the expression of Nuclear factor of activated T cells c1 (NFATc1) or SOX9 were investigated by quantitative reverse-transcription polymerase chain reaction, immunoblot, and immunohistochemical analyses of mouse and human tissues and acinar cell explants.

group-Box gene 9 (Sox9), one of the earliest markers of committed chondrogenic cells, is reduced in Ca v3.2 −/ tracheas. Mechanistically, Ca2+ influx via Ca v3.2 activates the calcineurin/nuclear factor of the activated T-cell (NFAT) signaling pathway, and a previously uniden-tified NFAT binding site is identified within the mouse Sox9 pro-

In this study, we first demonstrated that RCAN1.4 is positively associated with disc degeneration and that hypoxia-induced downregulation of RCAN1.4 activated the calcineurin/NFAT signaling pathway to facilitate SOX9 and MMP13 expression. Furthermore, NFATc1 could directly bind the promotor regions of SOX9 and MMP13.