| pubmed-article:16109714 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16109714 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:16109714 | lifeskim:mentions | umls-concept:C0521447 | lld:lifeskim |
| pubmed-article:16109714 | lifeskim:mentions | umls-concept:C0333516 | lld:lifeskim |
| pubmed-article:16109714 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:16109714 | lifeskim:mentions | umls-concept:C1335671 | lld:lifeskim |
| pubmed-article:16109714 | lifeskim:mentions | umls-concept:C1847321 | lld:lifeskim |
| pubmed-article:16109714 | lifeskim:mentions | umls-concept:C1521761 | lld:lifeskim |
| pubmed-article:16109714 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:16109714 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:16109714 | pubmed:issue | 42 | lld:pubmed |
| pubmed-article:16109714 | pubmed:dateCreated | 2005-10-17 | lld:pubmed |
| pubmed-article:16109714 | pubmed:abstractText | Osteoclast differentiation from hematopoietic precursors is controlled by the tumor necrosis factor family member tumor necrosis factor-related activation-induced cytokine (TRANCE) via induction of various transcription factors, including nuclear factor of activated T cells (NFAT) c1. During osteoclast differentiation, NFATc1 is further activated via calcium signaling when costimulatory receptors expressed on osteoclast precursors, such as osteoclast-associated receptor (OSCAR), are stimulated. Here we show that NFATc1 expression precedes that of OSCAR during TRANCE-mediated osteoclastogenesis and that inhibition of NFATc1 by cyclosporin A abolishes TRANCE-induced OSCAR expression and subsequent osteoclast differentiation. Moreover, we show that the 1.0-kb promoter region of the OSCAR gene contains three potential NFATc1-binding sites. Induction of an OSCAR promoter-luciferase reporter is significantly increased when transiently transfected into 293T cells in combination with NFATc1 expression plasmid. Deletion and site-directed mutant constructs confirmed that NFATc1-binding sites are both functional and NFATc1-specific. Furthermore, NFATc1 synergistically activates an OSCAR reporter construct together with microphthalmia transcription factor and PU.1, transcription factors previously shown to be critical for osteoclast differentiation. In addition, a plasmid expressing constitutively active MAP kinase kinase 6 enhances the transactivation activity of NFATc1/microphthalmia transcription factor/PU.1 on the OSCAR promoter. Taken together, our results indicate that NFATc1 is an important transcription factor in the induction of OSCAR during osteoclastogenesis. Elucidation of NFATc1 as a transcription factor for OSCAR expression implies the presence of a positive feedback circuit of TRANCE-induced activation of NFATc1, involving NFATc1-mediated OSCAR expression and its subsequent activation of NFATc1, necessary for efficient differentiation of osteoclasts. | lld:pubmed |
| pubmed-article:16109714 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16109714 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16109714 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16109714 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:16109714 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:16109714 | pubmed:author | pubmed-author:TseLL | lld:pubmed |
| pubmed-article:16109714 | pubmed:author | pubmed-author:FisherDavid... | lld:pubmed |
| pubmed-article:16109714 | pubmed:author | pubmed-author:ChoiYongwonY | lld:pubmed |
| pubmed-article:16109714 | pubmed:author | pubmed-author:KimKyung... | lld:pubmed |
| pubmed-article:16109714 | pubmed:author | pubmed-author:KimNacksungN | lld:pubmed |
| pubmed-article:16109714 | pubmed:author | pubmed-author:KimJung HaJH | lld:pubmed |
| pubmed-article:16109714 | pubmed:author | pubmed-author:JinHye-MiHM | lld:pubmed |
| pubmed-article:16109714 | pubmed:author | pubmed-author:KimKabsunK | lld:pubmed |
| pubmed-article:16109714 | pubmed:author | pubmed-author:LeeJunwonJ | lld:pubmed |
| pubmed-article:16109714 | pubmed:author | pubmed-author:LeeSeoung-Hoo... | lld:pubmed |
| pubmed-article:16109714 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16109714 | pubmed:day | 21 | lld:pubmed |
| pubmed-article:16109714 | pubmed:volume | 280 | lld:pubmed |
| pubmed-article:16109714 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16109714 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16109714 | pubmed:pagination | 35209-16 | lld:pubmed |
| pubmed-article:16109714 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:16109714 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:16109714 | pubmed:articleTitle | Nuclear factor of activated T cells c1 induces osteoclast-associated receptor gene expression during tumor necrosis factor-related activation-induced cytokine-mediated osteoclastogenesis. | lld:pubmed |
| pubmed-article:16109714 | pubmed:affiliation | Medical Research Center for Gene Regulation, Chonnam National University Medical School, Gwangju, 501-746, Korea. | lld:pubmed |
| pubmed-article:16109714 | pubmed:publicationType | Journal Article | lld:pubmed |
