Regulation of NFATc1 in Osteoclast Differentiation.
10.11005/jbm.2014.21.4.233
- Author:
Jung Ha KIM
1
;
Nacksung KIM
Author Information
1. Department of Pharmacology, Medical Research Center for Gene Regulation, Chonnam National University Medical School, Gwangju, Korea. nacksung@jnu.ac.kr
- Publication Type:Review
- Keywords:
Gene expression regulation;
NFATc transcription factors;
Osteoclasts;
RANK ligand
- MeSH:
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
- From:Journal of Bone Metabolism
2014;21(4):233-241
- CountryRepublic of Korea
- Language:English
-
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.
