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
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 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.
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
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
Jung Ha Kim, Kabsun Kim, Inyoung Kim, Semun Seong, and Nacksung Kim
Mol. Cells 2015; 38(10): 904-910 https://doi.org/10.14348/molcells.2015.0177Kabsun Kim, Jung Ha Kim, Inyoung Kim, Jongwon Lee, Semun Seong, Yong-Wook Park, and Nacksung Kim
Mol. Cells 2015; 38(1): 75-80 https://doi.org/10.14348/molcells.2015.2241Kabsun Kim*, Jung Ha Kim, Jang Bae Moon, Jongwon Lee, Han bok Kwak, Yong-Wook Park,and Nacksung Kim*
Mol. Cells 2012; 33(4): 401-406 https://doi.org/10.1007/s10059-012-0009-2