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http://purl.uniprot.org/citations/12372427http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/12372427http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/12372427http://www.w3.org/2000/01/rdf-schema#comment"Analysis of patients with atopic dermatitis (AD) for differential expression of genes, as compared to normal individuals, will be useful for understanding the molecular pathogenesis of AD. We found that the expression of the gene ETEA in human peripheral blood CD3-positive cells from patients with atopic dermatitis was significantly higher than in normal individuals. Eosinophils from AD patients expressed ETEA at a significantly higher level than the healthy controls. The overall sequence of the 445 aa deduced polypeptide from the cloned ETEA cDNA showed homology to human Fas-associated factor 1 (FAF1), which is involved in Fas-mediated apoptosis. However, the interaction of ETEA with the Fas death domain was weaker than that of FAF1, as studied in yeast two-hybrid experiments. The ETEA-EGFP fusion protein was expressed in cytoplasm. During the course of activation-induced cell death of primary T cells, transcription levels of ETEA and FAF1 were upregulated with similar kinetics. The enhanced expression of ETEA may play a role in the regulating the resistance to apoptosis that is observed in T cells and eosinophils of AD patients."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.org/dc/terms/identifier"doi:10.1016/s0006-291x(02)02380-x"xsd:string
http://purl.uniprot.org/citations/12372427http://purl.org/dc/terms/identifier"doi:10.1016/s0006-291x(02)02380-x"xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Akasawa A."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Akasawa A."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Imai Y."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Imai Y."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Matsumoto K."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Matsumoto K."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Tanaka T."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Tanaka T."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Saito H."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Saito H."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Oshida T."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Oshida T."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Tsujimoto G."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Tsujimoto G."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Sugita Y."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Sugita Y."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Hashida R."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Hashida R."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Nakada A."xsd:string
http://purl.uniprot.org/citations/12372427http://purl.uniprot.org/core/author"Nakada A."xsd:string