Open AccessMedicineBiology

Jung Ha Kim, Nacksung Kim

2014.11.1Journal of Bone Metabolism

DOI: 10.11005/jbm.2014.21.4.233

tlooto Summary

Several mechanisms, including transcription, methylation, ubiquitination, acetylation, and non-coding RNAs, have been shown to regulate expression and activation of NFATc1, which plays the role of a master transcription regulator of osteoclast differentiation.

Abstract

Osteoclasts are unique cells that degrade the bone matrix. These large multinucleated cells differentiate from the monocyte/macrophage lineage upon stimulation by two essential cytokines, macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-kappa B (NF-κB) ligand (RANKL). Activation of transcription factors such as microphthalmia transcription factor (MITF), c-Fos, NF-κB, and nuclear factor-activated T cells c1 (NFATc1) is required for sufficient osteoclast differentiation. In particular, NFATc1 plays the role of a master transcription regulator of osteoclast differentiation. To date, several mechanisms, including transcription, methylation, ubiquitination, acetylation, and non-coding RNAs, have been shown to regulate expression and activation of NFATc1. In this review, we have summarized the various mechanisms that control NFATc1 regulation during osteoclast differentiation.

Citation format

KIM, Jung Ha; KIM, Nacksung. Regulation of nfatc1 in osteoclast differentiation. Journal of Bone Metabolism, 2014, 21: 233–241.