| Aberrant signalling and transcription factor activation as an explanation for the defective growth control and differentiation of keratinocytes in psoriasis: a hypothesis. | |
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MedLine Citation:
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PMID: 12930288 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Psoriasis is a chronic inflammatory skin disease characterized by the accumulation of red, scaly plaques on the skin. The plaques result from hyperproliferation and incomplete differentiation of keratinocytes (KC) in a process that seems to be driven, in part by skin-infiltrating leucocytes. We believe that the KC have inherent defects in intracellular signalling which could be usefully targeted to allow the development of more effective therapies. We suggest that there are defects in the regulation of the transcription factors: signal transducer and activator of transcription (STAT-1alpha), interferon regulated factor-1 (IRF-1) and NFkappaB which lead to loss of growth and differentiation control when the cells are subjected to physico-chemical and immunological stress. We also highlight recent studies that suggest that peroxisome proliferator-activated receptors, the notch receptor and defects in calcium and other ion transporting proteins may contribute to impairment in the ability of psoriatic KC to differentiate. The role of these systems in the development of the psoriatic phenotype and tests of these hypotheses are proposed. |
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Authors:
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R C McKenzie; E Sabin |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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Title: Experimental dermatology Volume: 12 ISSN: 0906-6705 ISO Abbreviation: Exp. Dermatol. Publication Date: 2003 Aug |
Date Detail:
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Created Date: 2003-08-21 Completed Date: 2004-05-03 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 9301549 Medline TA: Exp Dermatol Country: Denmark |
Other Details:
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Languages: eng Pagination: 337-45 Citation Subset: IM |
Affiliation:
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Epidermal Inflammation and Protection Group, Department of Dermatology, University of Edinburgh, Edinburgh, Scotland, UK. Roddie.McKenzie@ed.ac.uk |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cell Differentiation Cell Division DNA-Binding Proteins / metabolism Humans Interferon Regulatory Factor-1 Interferon-Stimulated Gene Factor 3 Keratinocytes / metabolism*, pathology* Membrane Proteins / metabolism Models, Biological* NF-kappa B / metabolism Phosphoproteins / metabolism Psoriasis / etiology, metabolism*, pathology* Receptors, Notch Signal Transduction Transcription Factor AP-1 / metabolism Transcription Factors / metabolism* |
| Chemical | |
Reg. No./Substance:
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0/DNA-Binding Proteins; 0/IRF1 protein, human; 0/Interferon Regulatory Factor-1; 0/Interferon-Stimulated Gene Factor 3; 0/Membrane Proteins; 0/NF-kappa B; 0/Phosphoproteins; 0/Receptors, Notch; 0/Transcription Factor AP-1; 0/Transcription Factors; 0/gamma interferon activation factor |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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