pubmed-article:21321929 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:21321929 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:21321929 | lifeskim:mentions | umls-concept:C1704928 | lld:lifeskim |
pubmed-article:21321929 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
pubmed-article:21321929 | lifeskim:mentions | umls-concept:C0031715 | lld:lifeskim |
pubmed-article:21321929 | lifeskim:mentions | umls-concept:C0221928 | lld:lifeskim |
pubmed-article:21321929 | lifeskim:mentions | umls-concept:C0033634 | lld:lifeskim |
pubmed-article:21321929 | lifeskim:mentions | umls-concept:C0033681 | lld:lifeskim |
pubmed-article:21321929 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
pubmed-article:21321929 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:21321929 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:21321929 | pubmed:dateCreated | 2011-6-1 | lld:pubmed |
pubmed-article:21321929 | pubmed:abstractText | We have previously demonstrated that in response to transforming growth factor ? (TGF?), Fli-1 activity is repressed through a series of sequential posttranslational modifications, consisting of protein kinase C? (PKC?)-induced Thr312 phosphorylation, acetylation by p300/CREB binding protein-associated factor, and detachment from the collagen promoter. The purpose of this study was to further investigate the upstream events that lead to Fli-1 phosphorylation in response to TGF?. | lld:pubmed |
pubmed-article:21321929 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21321929 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21321929 | pubmed:language | eng | lld:pubmed |
pubmed-article:21321929 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21321929 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:21321929 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:21321929 | pubmed:month | Jun | lld:pubmed |
pubmed-article:21321929 | pubmed:issn | 1529-0131 | lld:pubmed |
pubmed-article:21321929 | pubmed:author | pubmed-author:AsanoYoshihid... | lld:pubmed |
pubmed-article:21321929 | pubmed:author | pubmed-author:TrojanowskaMa... | lld:pubmed |
pubmed-article:21321929 | pubmed:author | pubmed-author:LafyatisRober... | lld:pubmed |
pubmed-article:21321929 | pubmed:author | pubmed-author:BujorAndreea... | lld:pubmed |
pubmed-article:21321929 | pubmed:author | pubmed-author:HainesPaulP | lld:pubmed |
pubmed-article:21321929 | pubmed:copyrightInfo | Copyright © 2011 by the American College of Rheumatology. | lld:pubmed |
pubmed-article:21321929 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:21321929 | pubmed:volume | 63 | lld:pubmed |
pubmed-article:21321929 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:21321929 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:21321929 | pubmed:pagination | 1729-37 | lld:pubmed |
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pubmed-article:21321929 | pubmed:year | 2011 | lld:pubmed |
pubmed-article:21321929 | pubmed:articleTitle | The c-Abl tyrosine kinase controls protein kinase C?-induced Fli-1 phosphorylation in human dermal fibroblasts. | lld:pubmed |
pubmed-article:21321929 | pubmed:affiliation | Boston University School of Medicine, Arthritis Center-Rheumatology, Boston, Massachusetts 02118, USA. | lld:pubmed |
pubmed-article:21321929 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:21321929 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:21321929 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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