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Mol. Cells 2013; 36(3): 252-257

Published online August 29, 2013

https://doi.org/10.1007/s10059-013-0159-x

© The Korean Society for Molecular and Cellular Biology

SLAT Negatively Regulates RANKL-Induced Osteoclast Differentiation

Bang Ung Youn, Kabsun Kim, Jung Ha Kim, Jongwon Lee, Jang Bae Moon, Inyoung Kim, Yong-Wook Park, and Nacksung Kim

Department of Pharmacology, Medical Research Center for Gene Regulation, Chonnam National University Medical School, Gwangju 501-746, Korea, 1Department of Rheumatology, Chonnam National University Medical School and Hospital, Gwangju 501-757, Korea

Received: May 27, 2013; Revised: July 2, 2013; Accepted: July 2, 2013

Abstract

RANKL induces the formation of osteoclasts, which are responsible for bone resorption. Herein, we investigated the role of SWAP-70-like adapter of T cells (SLAT) in RANKL-induced osteoclastogenesis. Expression levels of SLAT were reduced during RANKL-induced osteoclastogenesis. Overexpression of SLAT in BMMs inhibited TRAP-positive multinuclear osteoclast formation and attenuated the expression of NFATc1, which is an important modulator in osteoclastogenesis. Furthermore, silencing of SLAT by RNA interference enhanced osteoclast formation as well as NFATc1 expression. In addition, SLAT was involved in RANKL-induced JNK activation in osteoclasts. Taken together, our data suggest that SLAT acts as a negative modulator of RANKL-induced osteoclastogenesis.

Keywords bone, gene expression, osteoclast differentiation, RANKL, SLAT

Article

Research Article

Mol. Cells 2013; 36(3): 252-257

Published online September 30, 2013 https://doi.org/10.1007/s10059-013-0159-x

Copyright © The Korean Society for Molecular and Cellular Biology.

SLAT Negatively Regulates RANKL-Induced Osteoclast Differentiation

Bang Ung Youn, Kabsun Kim, Jung Ha Kim, Jongwon Lee, Jang Bae Moon, Inyoung Kim, Yong-Wook Park, and Nacksung Kim

Department of Pharmacology, Medical Research Center for Gene Regulation, Chonnam National University Medical School, Gwangju 501-746, Korea, 1Department of Rheumatology, Chonnam National University Medical School and Hospital, Gwangju 501-757, Korea

Received: May 27, 2013; Revised: July 2, 2013; Accepted: July 2, 2013

Abstract

RANKL induces the formation of osteoclasts, which are responsible for bone resorption. Herein, we investigated the role of SWAP-70-like adapter of T cells (SLAT) in RANKL-induced osteoclastogenesis. Expression levels of SLAT were reduced during RANKL-induced osteoclastogenesis. Overexpression of SLAT in BMMs inhibited TRAP-positive multinuclear osteoclast formation and attenuated the expression of NFATc1, which is an important modulator in osteoclastogenesis. Furthermore, silencing of SLAT by RNA interference enhanced osteoclast formation as well as NFATc1 expression. In addition, SLAT was involved in RANKL-induced JNK activation in osteoclasts. Taken together, our data suggest that SLAT acts as a negative modulator of RANKL-induced osteoclastogenesis.

Keywords: bone, gene expression, osteoclast differentiation, RANKL, SLAT

Mol. Cells
Nov 30, 2023 Vol.46 No.11, pp. 655~725
COVER PICTURE
Kim et al. (pp. 710-724) demonstrated that a pathogen-derived Ralstonia pseudosolanacearum type III effector RipL delays flowering time and enhances susceptibility to bacterial infection in Arabidopsis thaliana. Shown is the RipL-expressing Arabidopsis plant, which displays general dampening of the transcriptional program during pathogen infection, grown in long-day conditions.

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