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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2011-6-1
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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?.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Collagen Type I,
http://linkedlifedata.com/resource/pubmed/chemical/FLII protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Microfilament Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Piperazines,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C-delta,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-abl,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrimidines,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cytoplasmic and Nuclear,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/imatinib
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1529-0131
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pubmed:author |
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pubmed:copyrightInfo |
Copyright © 2011 by the American College of Rheumatology.
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pubmed:issnType |
Electronic
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pubmed:volume |
63
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1729-37
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pubmed:meshHeading |
pubmed-meshheading:21321929-Cell Nucleus,
pubmed-meshheading:21321929-Cells, Cultured,
pubmed-meshheading:21321929-Collagen Type I,
pubmed-meshheading:21321929-Dermis,
pubmed-meshheading:21321929-Female,
pubmed-meshheading:21321929-Fibroblasts,
pubmed-meshheading:21321929-Humans,
pubmed-meshheading:21321929-Male,
pubmed-meshheading:21321929-Microfilament Proteins,
pubmed-meshheading:21321929-Phosphorylation,
pubmed-meshheading:21321929-Piperazines,
pubmed-meshheading:21321929-Protein Kinase C-delta,
pubmed-meshheading:21321929-Protein Kinase Inhibitors,
pubmed-meshheading:21321929-Proto-Oncogene Proteins c-abl,
pubmed-meshheading:21321929-Pyrimidines,
pubmed-meshheading:21321929-RNA, Small Interfering,
pubmed-meshheading:21321929-Receptors, Cytoplasmic and Nuclear,
pubmed-meshheading:21321929-Scleroderma, Systemic,
pubmed-meshheading:21321929-Transduction, Genetic,
pubmed-meshheading:21321929-Transforming Growth Factor beta
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pubmed:year |
2011
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pubmed:articleTitle |
The c-Abl tyrosine kinase controls protein kinase C?-induced Fli-1 phosphorylation in human dermal fibroblasts.
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pubmed:affiliation |
Boston University School of Medicine, Arthritis Center-Rheumatology, Boston, Massachusetts 02118, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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