MafB negatively regulates RANKL-mediated osteoclast differentiation

Kabsun Kim, Ha Kim Jung, Junwon Lee, Mi Jin Hye, Hyun Kook, Keun Kim Kyung, Young Lee Soo, Nacksung Kim

Research output: Contribution to journalArticlepeer-review

227 Scopus citations


Receptor activator of nuclear factor κB ligand (RANKL) induces osteoclast formation from hematopoietic cells via regulation of various transcription factors. Here, we show that MafB negatively regulates RANKL-induced osteoclast differentiation. Expression levels of MafB are significantly reduced by RANKL during osteoclastogenesis. Overexpression of MafB in bone marrow-derived monocyte/macrophage lineage cells (BMMs) inhibits the formation of TRAP+ multinuclear osteoclasts, but phagocytic activity of BMMs is retained. Furthermore, overexpression of MafB in BMMs attenuates the gene induction of NFATc1 and osteoclast-associated receptor (OSCAR) during RANKL-mediated osteoclastogenesis. In addition, MafB proteins interfere with the DNA-binding ability of c-Fos, Mitf, and NFATc1, inhibiting their transactivation of NFATc1 and OSCAR. Furthermore, reduced expression of MafB by RNAi enhances osteoclastogenesis and increases expression of NFATc1 and OSCAR. Taken together, our results suggest that MafB can act as an important modulator of RANKL-mediated osteoclastogenesis.

Original languageEnglish
Pages (from-to)3253-3259
Number of pages7
Issue number8
StatePublished - 15 Apr 2007


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