BMB Reports Papers in Press available online.

Search Papers In Press
This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

Actin-binding LIM Protein 1 Regulates Receptor Activator of NF-リB Ligand-Mediated Osteoclast Differentiation and Motility
Su Hyun Jin1, Hyunsoo Kim2, Dong Ryun Gu1,3, Keun Ha Park1,3, Young Rae Lee1,4,5, Yongwon Choi2, Seoung Hoon Lee1,3,5,*
1Center for Metabolic Function Regulation (CMFR), Wonkwang University School of Medicine,
2Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine,
3Oral Microbiology and Immunology and 4Oral Biochemistry and 5Institute of Biomaterials∙Implant, College of Dentistry, Wonkwang University
Actin-binding LIM protein 1 (ABLIM1), a member of the LIM-domain protein family, mediates interactions between actin filaments and cytoplasmic targets. However, the role of ABLIM1 in osteoclast and bone metabolism has not been reported. In the present study, we investigated the role of ABLIM1 in receptor activator of NF-リB ligand (RANKL)-mediated osteoclastogenesis. ABLIM1 expression was induced by RANKL treatment and knockdown of ABLIM1 by retrovirus infection containing Ablim1-specific short hairpin RNA (shAblim1) decreased mature osteoclast formation and bone resorption activity in a RANKL-dose dependent manner. Coincident with the downregulated expression of osteoclast differentiation marker genes, the expression levels of c-Fos and nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), critical transcription factors of osteoclastogenesis, were also decreased in shAblim1-infected osteoclasts during RANKL-mediated osteoclast differentiation. In addition, the motility of preosteoclast was reduced by ABLIM1 knockdown via modulation of the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/Akt/Rac1 signaling pathway, suggesting another regulatory mechanism of ABLIM1 in osteoclast formation. These data demonstrated that ABLIM1 is a positive regulator of RANKL-mediated osteoclast formation via modulation of differentiation and PI3K/Akt/Rac1-dependent motility.
Abstract, Accepted Manuscript(in press) [Submitted on May 11, 2018, Accepted on May 29, 2018]
  Copyright © KSBMB. All rights reserved. / Powered by, Ltd