| pubmed-article:9988737 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9988737 | lifeskim:mentions | umls-concept:C0162508 | lld:lifeskim |
| pubmed-article:9988737 | lifeskim:mentions | umls-concept:C0246120 | lld:lifeskim |
| pubmed-article:9988737 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:9988737 | pubmed:dateCreated | 1999-3-18 | lld:pubmed |
| pubmed-article:9988737 | pubmed:abstractText | The ETS domain transcription factor PU.1 is necessary for the development of monocytes and regulates, in particular, the expression of the monocyte-specific macrophage colony-stimulating factor (M-CSF) receptor, which is critical for monocytic cell survival, proliferation, and differentiation. The bZIP transcription factor c-Jun, which is part of the AP-1 transcription factor complex, is also important for monocytic differentiation, but the monocyte-specific M-CSF receptor promoter has no AP-1 consensus binding sites. We asked the question of whether c-Jun could promote the induction of the M-CSF receptor by collaborating with PU.1. We demonstrate that c-Jun enhances the ability of PU.1 to transactivate the M-CSF receptor promoter as well as a minimal thymidine kinase promoter containing only PU.1 DNA binding sites. c-Jun does not directly bind to the M-CSF receptor promoter but associates via its basic domain with the ETS domain of PU.1. Consistent with our observation that AP-1 binding does not contribute to c-Jun coactivation is the observation that the activation of PU.1 by c-Jun is blocked by overexpression of c-Fos. Phosphorylation of c-Jun by c-Jun NH2-terminal kinase on Ser-63 and -73 does not alter the ability of c-Jun to enhance PU.1 transactivation. Activated Ras enhances the transcriptional activity of PU.1 by up-regulating c-Jun expression without changing the phosphorylation pattern of PU.1. The activation of PU.1 by Ras is blocked by a mutant c-Jun protein lacking the basic domain. The expression of this mutant form of c-Jun also completely blocks 12-O-tetradecanoylphorbol-13-acetate-induced M-CSF receptor promoter activity during monocytic differentiation. We propose therefore that c-Jun acts as a c-Jun NH2-terminal kinase-independent coactivator of PU.1, resulting in M-CSF receptor expression and development of the monocytic lineage. | lld:pubmed |
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| pubmed-article:9988737 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9988737 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9988737 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9988737 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:9988737 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:9988737 | pubmed:author | pubmed-author:TenenD GDG | lld:pubmed |
| pubmed-article:9988737 | pubmed:author | pubmed-author:DavisR JRJ | lld:pubmed |
| pubmed-article:9988737 | pubmed:author | pubmed-author:CarpenterC... | lld:pubmed |
| pubmed-article:9988737 | pubmed:author | pubmed-author:CoghlanM PMP | lld:pubmed |
| pubmed-article:9988737 | pubmed:author | pubmed-author:HoangTT | lld:pubmed |
| pubmed-article:9988737 | pubmed:author | pubmed-author:ZhengH MHM | lld:pubmed |
| pubmed-article:9988737 | pubmed:author | pubmed-author:BehreGG | lld:pubmed |
| pubmed-article:9988737 | pubmed:author | pubmed-author:WhitmarshA... | lld:pubmed |
| pubmed-article:9988737 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9988737 | pubmed:day | 19 | lld:pubmed |
| pubmed-article:9988737 | pubmed:volume | 274 | lld:pubmed |
| pubmed-article:9988737 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9988737 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9988737 | pubmed:pagination | 4939-46 | lld:pubmed |
| pubmed-article:9988737 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:9988737 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:9988737 | pubmed:articleTitle | c-Jun is a JNK-independent coactivator of the PU.1 transcription factor. | lld:pubmed |
| pubmed-article:9988737 | pubmed:affiliation | Division of Hematology/Oncology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02115, USA. | lld:pubmed |
| pubmed-article:9988737 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9988737 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:9988737 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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