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Runx2 phosphorylation induced by fibroblast growth factor-2/protein kinase C pathways

Cited 77 time in Web of Science Cited 80 time in Scopus
Authors
Ryoo, Hyun-Mo; Kim, Byung-Gyu; Kim, Hyun-Jung; Park, Hye-Jeong; Kim, Youn-Jeong; Yoon, Won-Joon; Lee, Seung-Jin; Cho, Je-Yoel
Issue Date
2006-01
Publisher
Wiley-Blackwell
Citation
Proteomics 2006, 6, 1166-1174
Keywords
Fibroblast growth factorFGF receptorMALDI-TOFPhosphorylationProtein kinase CRunx2
Abstract
Runx2 is a key transcription factor in osteoblast differentiation, and its activity is regulated by fibroblast growth factors (FGFs). Craniosynostosis, characterized by premature suture closure, results from mutations that generate constitutively active FGF receptors (FGFRs). We previously showed that FGF/FGFR-activated protein kinase C (PKC) is involved in the expression and activity of Runx2. Activated PKC physically interacts with Runx2 in FGF2-stimulated MC3T3-E1 preosteoblastic cells. Immunopurified Runx2 protein reacted with PKC kinase, and a phosphorylated 1460-Da peptide fragment (amino acids 241-252, 1380-Da) derived from Runx2 was also detected in MS analysis. Computer analysis predicted that Ser247 in this Runx2 can be a possible phosphorylation site by PKC. We also showed that Runx2 activity after FGF stimulation correlates with the presence of the Runx2 Ser247 residue. The S247A (Ser Ala) mutation confers decreased transcriptional activity on a Runx2-responsive promoter after FGF treatment.
ISSN
1615-9853
Language
English
URI
http://hdl.handle.net/10371/69663
DOI
https://doi.org/10.1002/pmic.200500289
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College of Dentistry/School of Dentistry (치과대학/치의학대학원)Dept. of Dentistry (치의학과)Journal Papers (저널논문_치의학과)
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