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Cited by 238

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

MafB negatively regulates RANKL-mediated osteoclast differentiation

Kim, Kabsun, Kim, Jung Ha, Lee, Junwon, Jin, Hye Mi, Kook, Hyun, Kim, Kyung Keun, Lee, Soo Young, Kim, Nacksung·2007·Blood

Abstract

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.

Overview

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Crossref · 10.1182/blood-2006-09-048249

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6 of 6 references verified0 citation errors · 0 not checkable

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Citations

Cites

Research works printed but not linked: 31

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Cited by

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Metadata

Authors
Kim, K., Kim, J. H., Lee, J., Jin, H. M., Kook, H., Kim, K. K., Lee, S. Y., & Kim, N.
Affiliations
  • Research Institute of Medical Sciences and Medical Research Center for Gene Regulation, Chonnam National University Medical School, Gwangju, Korea;
  • Division of Molecular Life Sciences and Center for Cell Signaling Research, Ewha Womans University, Seoul, Korea
Venue
Blood
Published
2006-12-07
Volume
109
Issue
8
Pages
3253-3259
ISSN
  • 0006-4971
  • 1528-0020
Cited by
238
References
6
Language
en

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