| pubmed-article:11114331 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11114331 | lifeskim:mentions | umls-concept:C1123023 | lld:lifeskim |
| pubmed-article:11114331 | lifeskim:mentions | umls-concept:C0162508 | lld:lifeskim |
| pubmed-article:11114331 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
| pubmed-article:11114331 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
| pubmed-article:11114331 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:11114331 | pubmed:dateCreated | 2000-12-18 | lld:pubmed |
| pubmed-article:11114331 | pubmed:abstractText | Interactions between mesenchymal and epithelial cells are responsible for organogenesis and tissue homeostasis. This mutual cross-talk involves cell surface proteins and soluble factors, which are mostly the result of regulated transcription. To elucidate dimer-specific functions of the AP-1 family of transcription factors, we reconstituted skin by combining primary human keratinocytes and mouse wild-type, c-jun(-/-), and junB(-/-) fibroblasts. We have discovered an antagonistic function of these AP-1 subunits in the fibroblast-mediated paracrine control of keratinocyte proliferation and differentiation, and traced this effect to the IL-1-dependent regulation of KGF and GM-CSF. These data suggest that the relative activation state of these AP-1 subunits in a non-cell-autonomous, transregulatory fashion directs regeneration of the epidermis and maintenance of tissue homeostasis in skin. | lld:pubmed |
| pubmed-article:11114331 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11114331 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11114331 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11114331 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:11114331 | pubmed:issn | 0092-8674 | lld:pubmed |
| pubmed-article:11114331 | pubmed:author | pubmed-author:FusenigN ENE | lld:pubmed |
| pubmed-article:11114331 | pubmed:author | pubmed-author:AngerVV | lld:pubmed |
| pubmed-article:11114331 | pubmed:author | pubmed-author:Maas-Szabowsk... | lld:pubmed |
| pubmed-article:11114331 | pubmed:author | pubmed-author:Schorpp-Kistn... | lld:pubmed |
| pubmed-article:11114331 | pubmed:author | pubmed-author:KolbusAA | lld:pubmed |
| pubmed-article:11114331 | pubmed:author | pubmed-author:SzabowskiAA | lld:pubmed |
| pubmed-article:11114331 | pubmed:author | pubmed-author:AndrechtSS | lld:pubmed |
| pubmed-article:11114331 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11114331 | pubmed:day | 22 | lld:pubmed |
| pubmed-article:11114331 | pubmed:volume | 103 | lld:pubmed |
| pubmed-article:11114331 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11114331 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11114331 | pubmed:pagination | 745-55 | lld:pubmed |
| pubmed-article:11114331 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:11114331 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:11114331 | pubmed:articleTitle | c-Jun and JunB antagonistically control cytokine-regulated mesenchymal-epidermal interaction in skin. | lld:pubmed |
| pubmed-article:11114331 | pubmed:affiliation | Division of Signal Transduction and Growth Control Deutsches Krebsforschungszentrum Im Neuenheimer Feld 280 69120, Heidelberg, Germany. | lld:pubmed |
| pubmed-article:11114331 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11114331 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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