| http://purl.uniprot.org/citations/19516260 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/19516260 | http://www.w3.org/2000/01/rdf-schema#comment | "We have shown earlier that inhibiting NF-kappaB activity in murine basal keratinocytes leads to hyperproliferation, inflammation, and cancer in a tumor necrosis factor receptor 1 (TNFR1)-dependent manner. We report here the outcomes of NF-kappaB abrogation at different stages of epidermal morphogenesis using a conditional IkappaBalpha transgenic mouse model. We find that blocking NF-kappaB during embryogenesis mimics the epidermal and glandular defects seen in the human disease hypohidrotic/anhidrotic ectodermal dysplasia (HED/EDA), independently of the inflammatory phenotype and TNFR1. The onset of transgene expression after birth correlates with nuclear exclusion of the NF-kappaB p50 subunit, hyperplasia, and development of a chronic inflammation initiated and dominated by macrophages. In this model, macrophages are important producers of the vascular endothelial growth factor A (VEGFA), whose inhibition attenuates the excessive angiogenesis otherwise observed. The inflammatory reaction requires the continuous suppression of NF-kappaB in keratinocytes, indicating that an immune cell attractant(s) is directly induced in response to NF-kappaB inhibition. As TNFalpha upregulation is a late event in this model, good candidates for such chemoattraction are the monocyte chemotactic proteins 1, 2, and 3 (MCP-1-2-3), which are upregulated in the epidermal compartment concomitantly with the onset of NF-kappaB inhibition."xsd:string |
| http://purl.uniprot.org/citations/19516260 | http://purl.org/dc/terms/identifier | "doi:10.1038/jid.2009.126"xsd:string |
| http://purl.uniprot.org/citations/19516260 | http://purl.uniprot.org/core/author | "Memet S."xsd:string |
| http://purl.uniprot.org/citations/19516260 | http://purl.uniprot.org/core/author | "Toftgard R."xsd:string |
| http://purl.uniprot.org/citations/19516260 | http://purl.uniprot.org/core/author | "Sur I."xsd:string |
| http://purl.uniprot.org/citations/19516260 | http://purl.uniprot.org/core/author | "Ulvmar M.H."xsd:string |
| http://purl.uniprot.org/citations/19516260 | http://purl.uniprot.org/core/date | "2009"xsd:gYear |
| http://purl.uniprot.org/citations/19516260 | http://purl.uniprot.org/core/name | "J Invest Dermatol"xsd:string |
| http://purl.uniprot.org/citations/19516260 | http://purl.uniprot.org/core/pages | "2584-2593"xsd:string |
| http://purl.uniprot.org/citations/19516260 | http://purl.uniprot.org/core/title | "Timed NF-kappaB inhibition in skin reveals dual independent effects on development of HED/EDA and chronic inflammation."xsd:string |
| http://purl.uniprot.org/citations/19516260 | http://purl.uniprot.org/core/volume | "129"xsd:string |
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