Background: Constitutive homozygous Men1-/- mice at mid-gestation are small with craniofacial defects. Results: Conditional osteoblast Men1 knock-out mice have reduced bone mass, and transgenic osteoblast menin-overexpressing mice have increased bone mass. Conclusion: Knock-out mice menin-deficient primary osteoblasts have impaired mineralization and reduced responsiveness to TGF-β and BMP-2. Significance: Menin is a potential target for gain of function therapeutics in low bone mass disorders.
CITATION STYLE
Kanazawa, I., Canaff, L., Rafeh, J. A., Angrula, A., Li, J., Riddle, R. C., … Hendy, G. N. (2015). Osteoblast menin regulates bone mass in vivo. Journal of Biological Chemistry, 290(7), 3910–3924. https://doi.org/10.1074/jbc.M114.629899
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