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dc.creatorTomicCanic, M
dc.creatorFreedberg, IM
dc.creatorBlumenberg, M
dc.date.accessioned2018-03-01T18:12:22Z
dc.date.available2018-03-01T18:12:22Z
dc.date.issued1996
dc.identifier.issn0014-4827 (print)
dc.identifier.urihttp://vinar.vin.bg.ac.rs/handle/123456789/1976
dc.description.abstractEpidermal keratinocytes are subject to a large variety of signals that modulate their differentiation in health and their activation in disease. Hormones and vitamins, which act via nuclear receptors, affect the differentiation process, whereas growth factors and cytokines, which act via cell surface receptors, affect keratinocyte activation and related events. Using expression of keratin genes as markers for keratinocyte phenotype, we examined the interaction between the nuclear receptor and cell surface receptor pathways. We expected to find dominance of one of the pathways. Surprisingly, we found that the two pathways are co-dominant. Specifically, while EGF induces expression of K6 and K16 keratin genes, retinoic acid suppresses their expression, and when both mediators are present simultaneously, the level of expression is intermediate, a product of both signals. Similar codominant effects were found on other keratin genes using interferon gamma, TGF beta, and thyroid hormone signaling molecules. These codominant effects are specific only for genes that are regulated by both pathways. Our results suggest that a judicious combination of hormones, vitamins, growth factors, and cytokines may be used to target specific expression of appropriate genes in the treatment of human epidermal diseases. (C) 1996 Academic Press, Inc.en
dc.relationNIAMS NIH HHS [AR40522, AR30682, AR39176]
dc.rightsrestrictedAccessen
dc.sourceExperimental Cell Researchen
dc.titleCodominant regulation of keratin gene expression by cell surface receptors and nuclear receptorsen
dc.typearticleen
dcterms.abstractТомицЦаниц, М; Фреедберг, ИМ; Блуменберг, М;
dc.citation.volume224
dc.citation.issue1
dc.citation.spage96
dc.citation.epage102
dc.identifier.wosA1996UH25100011
dc.identifier.doi10.1006/excr.1996.0115
dc.identifier.pmid8612697
dc.identifier.scopus2-s2.0-17644441891


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