Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 배윤수 | * |
dc.contributor.author | 이수영 | * |
dc.date.accessioned | 2018-05-18T08:14:55Z | - |
dc.date.available | 2018-05-18T08:14:55Z | - |
dc.date.issued | 2005 | * |
dc.identifier.issn | 0006-4971 | * |
dc.identifier.other | OAK-2855 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/243067 | - |
dc.description.abstract | Signaling by receptor activator of NF-κB (nuclear factor-κB) ligand (RANKL) is essential for differentiation of bone marrow monocyte-macrophage lineage (BMM) cells into osteoclasts. Here, we show RANKL stimulation of BMM cells transiently increased the intracellular level of reactive oxygen species (ROS) through a signaling cascade involving TNF (tumor necrosis factor) receptor-associated factor (TRAF) 6, Rac1, and NADPH (nicotinamide adenine dinucleotide phosphate) oxidase (Nox)1. A deficiency in TRAF6 or expression of a dominant-interfering mutant of TRAF6 blocks RANKL-mediated ROS production. Application of N-acetyl-cysteine (NAC) or blocking the activity of Nox, a protein leading to the formation of ROS, with diphenylene iodonium (DPI) inhibits the responses of BMM cells to RANKL, including ROS production, activation of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein (MAP) kinase, and extracellular signal-regulated kinase (ERK), and osteoclast differentiation. Moreover, both RANKL-mediated ROS production and osteoclast differentiation were completely blocked in precursors depleted of Nox1 activity by RNA interference or by expressing a dominant-negative mutant of Rac1. Together, these results indicate that ROSs act as an intracellular signal mediator for osteoclast differentiation. © 2005 by The American Society of Hematology. | * |
dc.language | English | * |
dc.title | A crucial role for reactive oxygen species in RANKL-induced osteoclast differentiation | * |
dc.type | Article | * |
dc.relation.issue | 3 | * |
dc.relation.volume | 106 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 852 | * |
dc.relation.lastpage | 859 | * |
dc.relation.journaltitle | Blood | * |
dc.identifier.doi | 10.1182/blood-2004-09-3662 | * |
dc.identifier.wosid | WOS:000230949100023 | * |
dc.identifier.scopusid | 2-s2.0-22144457305 | * |
dc.author.google | Lee N.K. | * |
dc.author.google | Choi Y.G. | * |
dc.author.google | Baik J.Y. | * |
dc.author.google | Han S.Y. | * |
dc.author.google | Jeong D.-W. | * |
dc.author.google | Bae Y.S. | * |
dc.author.google | Kim N. | * |
dc.author.google | Lee S.Y. | * |
dc.contributor.scopusid | 배윤수(15031067200) | * |
dc.contributor.scopusid | 이수영(53980218900;7409697278) | * |
dc.date.modifydate | 20240415133331 | * |