The ubiquitin-mediated degradation of Jak1 modulates osteoclastogenesis by limiting interferon-beta-induced inhibitory signaling
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, Youngkyun | - |
dc.contributor.author | Hyung, Seok-Won | - |
dc.contributor.author | Jung, Hee Jung | - |
dc.contributor.author | Kim, Hyung-Joon | - |
dc.contributor.author | Staerk, Judith | - |
dc.contributor.author | Constantinescu, Stefan N. | - |
dc.contributor.author | Chang, Eun-Ju | - |
dc.contributor.author | Lee, Zang Hee | - |
dc.contributor.author | Lee, Sang-Won | - |
dc.contributor.author | Kim, Hong-Hee | - |
dc.date.accessioned | 2021-09-09T12:40:59Z | - |
dc.date.available | 2021-09-09T12:40:59Z | - |
dc.date.created | 2021-06-15 | - |
dc.date.issued | 2008-01-15 | - |
dc.identifier.issn | 0006-4971 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/124435 | - |
dc.description.abstract | Interferons (IFNs) have been shown to negatively regulate osteoclastogenesis. In a proteomic study to assess protein expression during osteoclastogenesis, we discovered that the expression level of Jak1 was significantly decreased during the early stage of osteoclast differentiation from mouse bone marrow macrophages (BMMs) upon stimulation with receptor activator of nuclear factor kappa B ligand (RANKL). RANKL induced Jak1 ubiquitination, and a proteasome inhibitor MG 132 efficiently blocked the RANKL-induced degradation of Jak1. The expression level of Jak1 correlated with the susceptibility of osteoclast precursors to the negative regulatory effects of IFN-beta on osteoclastogenesis, since preosteoclasts (pOCs) in which Jak1 expression is significantly reduced could proceed with osteoclastogenesis in the presence of IFN-beta. Forced down-regulation of Jak1 by small interfering RNA (siRNA) resulted in the efficient osteoclast differentiation of BMMs in the presence of inhibitory IFN-beta, while overexpression of Jak1 in pOCs elicited IFN-beta-dependent inhibition of osteoclastogenesis. Furthermore, we found that the IFN-beta-induced inhibition of osteoclastogenesis required STAT3 downstream of Jak1. These data suggest that the regulation of Jak1 expression during osteoclast differentiation might serve as an intrinsic mechanism that determines osteoclast lineage commitment by modulating the negative regulation by IFN-beta. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | AMER SOC HEMATOLOGY | - |
dc.subject | FACTOR-KAPPA-B | - |
dc.subject | RECEPTOR ACTIVATOR | - |
dc.subject | RHEUMATOID-ARTHRITIS | - |
dc.subject | CROSS-TALK | - |
dc.subject | DIFFERENTIATION | - |
dc.subject | CELL | - |
dc.subject | SUPPRESSORS | - |
dc.subject | EXPRESSION | - |
dc.subject | RANKL | - |
dc.subject | COMMITMENT | - |
dc.title | The ubiquitin-mediated degradation of Jak1 modulates osteoclastogenesis by limiting interferon-beta-induced inhibitory signaling | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Lee, Sang-Won | - |
dc.identifier.doi | 10.1182/blood-2007-03-082941 | - |
dc.identifier.scopusid | 2-s2.0-38349118587 | - |
dc.identifier.wosid | 000252458700064 | - |
dc.identifier.bibliographicCitation | BLOOD, v.111, no.2, pp.885 - 893 | - |
dc.relation.isPartOf | BLOOD | - |
dc.citation.title | BLOOD | - |
dc.citation.volume | 111 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 885 | - |
dc.citation.endPage | 893 | - |
dc.type.rims | ART | - |
dc.type.docType | Review | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Hematology | - |
dc.relation.journalWebOfScienceCategory | Hematology | - |
dc.subject.keywordPlus | FACTOR-KAPPA-B | - |
dc.subject.keywordPlus | RECEPTOR ACTIVATOR | - |
dc.subject.keywordPlus | RHEUMATOID-ARTHRITIS | - |
dc.subject.keywordPlus | CROSS-TALK | - |
dc.subject.keywordPlus | DIFFERENTIATION | - |
dc.subject.keywordPlus | CELL | - |
dc.subject.keywordPlus | SUPPRESSORS | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | RANKL | - |
dc.subject.keywordPlus | COMMITMENT | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
(02841) 서울특별시 성북구 안암로 14502-3290-1114
COPYRIGHT © 2021 Korea University. All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.