Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이수영 | * |
dc.date.accessioned | 2021-06-07T16:31:24Z | - |
dc.date.available | 2021-06-07T16:31:24Z | - |
dc.date.issued | 2021 | * |
dc.identifier.issn | 2041-1723 | * |
dc.identifier.other | OAK-29372 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/257619 | - |
dc.description.abstract | Selenoproteins containing selenium in the form of selenocysteine are critical for bone remodeling. However, their underlying mechanism of action is not fully understood. Herein, we report the identification of selenoprotein W (SELENOW) through large-scale mRNA profiling of receptor activator of nuclear factor (NF)-κΒ ligand (RANKL)-induced osteoclast differentiation, as a protein that is downregulated via RANKL/RANK/tumour necrosis factor receptor-associated factor 6/p38 signaling. RNA-sequencing analysis revealed that SELENOW regulates osteoclastogenic genes. SELENOW overexpression enhances osteoclastogenesis in vitro via nuclear translocation of NF-κB and nuclear factor of activated T-cells cytoplasmic 1 mediated by 14-3-3γ, whereas its deficiency suppresses osteoclast formation. SELENOW-deficient and SELENOW-overexpressing mice exhibit high bone mass phenotype and osteoporosis, respectively. Ectopic SELENOW expression stimulates cell-cell fusion critical for osteoclast maturation as well as bone resorption. Thus, RANKL-dependent repression of SELENOW regulates osteoclast differentiation and blocks osteoporosis caused by overactive osteoclasts. These findings demonstrate a biological link between selenium and bone metabolism. © 2021, The Author(s). | * |
dc.language | English | * |
dc.publisher | Nature Research | * |
dc.title | Selenoprotein W ensures physiological bone remodeling by preventing hyperactivity of osteoclasts | * |
dc.type | Article | * |
dc.relation.issue | 1 | * |
dc.relation.volume | 12 | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.journaltitle | Nature Communications | * |
dc.identifier.doi | 10.1038/s41467-021-22565-7 | * |
dc.identifier.wosid | WOS:000641850800007 | * |
dc.identifier.scopusid | 2-s2.0-85104384851 | * |
dc.author.google | Kim H. | * |
dc.author.google | Lee K. | * |
dc.author.google | Kim J.M. | * |
dc.author.google | Kim M.Y. | * |
dc.author.google | Kim J.-R. | * |
dc.author.google | Lee H.-W. | * |
dc.author.google | Chung Y.W. | * |
dc.author.google | Shin H.-I. | * |
dc.author.google | Kim T. | * |
dc.author.google | Park E.-S. | * |
dc.author.google | Rho J. | * |
dc.author.google | Lee S.H. | * |
dc.author.google | Kim N. | * |
dc.author.google | Lee S.Y. | * |
dc.author.google | Choi Y. | * |
dc.author.google | Jeong D. | * |
dc.contributor.scopusid | 이수영(53980218900;7409697278) | * |
dc.date.modifydate | 20240415140424 | * |