J Bone Metab.  2014 Nov;21(4):233-241. 10.11005/jbm.2014.21.4.233.

Regulation of NFATc1 in Osteoclast Differentiation

Affiliations
  • 1Department of Pharmacology, Medical Research Center for Gene Regulation, Chonnam National University Medical School, Gwangju, Korea. nacksung@jnu.ac.kr

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-kappaB) ligand (RANKL). Activation of transcription factors such as microphthalmia transcription factor (MITF), c-Fos, NF-kappaB, 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.

Keyword

Gene expression regulation; NFATc transcription factors; Osteoclasts; RANK ligand

MeSH Terms

Acetylation
Bone Matrix
Cytokines
Gene Expression Regulation
Macrophage Colony-Stimulating Factor
Methylation
Microphthalmos
NF-kappa B
NFATC Transcription Factors
Osteoclasts*
RANK Ligand
Receptor Activator of Nuclear Factor-kappa B
RNA, Untranslated
T-Lymphocytes
Transcription Factors
Ubiquitin
Ubiquitination
Cytokines
Macrophage Colony-Stimulating Factor
NF-kappa B
NFATC Transcription Factors
RANK Ligand
RNA, Untranslated
Receptor Activator of Nuclear Factor-kappa B
Transcription Factors
Ubiquitin
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