pubmed-article:17885208 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17885208 | lifeskim:mentions | umls-concept:C0029431 | lld:lifeskim |
pubmed-article:17885208 | lifeskim:mentions | umls-concept:C0041904 | lld:lifeskim |
pubmed-article:17885208 | lifeskim:mentions | umls-concept:C0332466 | lld:lifeskim |
pubmed-article:17885208 | lifeskim:mentions | umls-concept:C0162493 | lld:lifeskim |
pubmed-article:17885208 | lifeskim:mentions | umls-concept:C1425406 | lld:lifeskim |
pubmed-article:17885208 | lifeskim:mentions | umls-concept:C1417694 | lld:lifeskim |
pubmed-article:17885208 | lifeskim:mentions | umls-concept:C1539977 | lld:lifeskim |
pubmed-article:17885208 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:17885208 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:17885208 | pubmed:dateCreated | 2007-12-31 | lld:pubmed |
pubmed-article:17885208 | pubmed:abstractText | NFATc1 has been characterized as a master regulator of nuclear factor kappaB ligand-induced osteoclast differentiation. Herein, we demonstrate a novel role for NFATc1 as a positive regulator of nuclear factor kappaB ligand-mediated osteoclast fusion as well as other fusion-inducing factors such as TNF-alpha. Exogenous overexpression of a constitutively active form of NFATc1 in bone marrow-derived monocyte/macrophage cells (BMMs) induces formation of multinucleated osteoclasts as well as the expression of fusion-mediating molecules such as the d2 isoform of vacuolar ATPase V(o) domain (Atp6v0d2) and the dendritic cell-specific transmembrane protein (DC-STAMP). Moreover, inactivation of NFATc1 by cyclosporin A treatment attenuates expression of Atp6v0d2 and DC-STAMP and subsequent fusion process of osteoclasts. We show that NFATc1 binds to the promoter regions of Atp6v0d2 and DC-STAMP in osteoclasts and directly induces their expression. Furthermore, overexpression of Atp6v0d2 and DC-STAMP rescues cell-cell fusion of preosteoclasts despite reduced NFATc1 activity. Our data indicate for the first time that the NFATc1/Atp6v0d2 and DC-STAMP signaling axis plays a key role in the osteoclast multinucleation process, which is essential for efficient bone resorption. | lld:pubmed |
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pubmed-article:17885208 | pubmed:language | eng | lld:pubmed |
pubmed-article:17885208 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17885208 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17885208 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17885208 | pubmed:month | Jan | lld:pubmed |
pubmed-article:17885208 | pubmed:issn | 0888-8809 | lld:pubmed |
pubmed-article:17885208 | pubmed:author | pubmed-author:ChoiYongwonY | lld:pubmed |
pubmed-article:17885208 | pubmed:author | pubmed-author:KimNacksungN | lld:pubmed |
pubmed-article:17885208 | pubmed:author | pubmed-author:KimKabsunK | lld:pubmed |
pubmed-article:17885208 | pubmed:author | pubmed-author:LeeSeoung-Hoo... | lld:pubmed |
pubmed-article:17885208 | pubmed:author | pubmed-author:Ha KimJungJ | lld:pubmed |
pubmed-article:17885208 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17885208 | pubmed:volume | 22 | lld:pubmed |
pubmed-article:17885208 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17885208 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17885208 | pubmed:pagination | 176-85 | lld:pubmed |
pubmed-article:17885208 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:17885208 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:17885208 | pubmed:articleTitle | NFATc1 induces osteoclast fusion via up-regulation of Atp6v0d2 and the dendritic cell-specific transmembrane protein (DC-STAMP). | lld:pubmed |
pubmed-article:17885208 | pubmed:affiliation | National Research Laboratory for Regulation of Bone Metabolism and Disease, Medical Research Center for Gene Regulation, Chonnam National University Medical School, Gwangju 501-746, Korea. | lld:pubmed |
pubmed-article:17885208 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17885208 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:17885208 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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