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The transcription factor early B-cell factor 1 regulates bone formation in an osteoblast-nonautonomous manner

MPG-Autoren
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Boller,  Sören
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Györy,  Ildiko
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Grosschedl,  Rudolf
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Externe Ressourcen

https://febs.onlinelibrary.wiley.com/doi/full/10.1016/j.febslet.2013.01.049
(Verlagsversion)

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Zitation

Zee, T., Boller, S., Györy, I., Tuckermann, J. P., Grosschedl, R., & Karsenty, G. (2013). The transcription factor early B-cell factor 1 regulates bone formation in an osteoblast-nonautonomous manner. FEBS Letters, 587, 711-716. doi:10.1016/j.febslet.2013.01.049.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-002B-8957-9
Zusammenfassung
Early B-cell factor 1 (Ebf1) is a transcription factor whose inactivation in all cells results in high bone mass because of an increase in bone formation. This observation suggests Ebf1 may be an inhibitor of osteoblast differentiation. To test this contention, we analyzed Ebf1 pattern of expression and function in osteoblasts ex vivo and in vivo through osteoblast-specific inactivation in the mouse. We show here that in vivo deletion of Ebf1 in osteoblast progenitors does not affect osteoblast differentiation or bone formation accrual post-natally. These observations indicate that the phenotype described in Ebf1-/- mice is not osteoblast-autonomous.