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A 1.8kb GFAP-promoter fragment is active in specific regions of theembryonic CNS
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology. (Tumorigenesis)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology. (Tumorigenesis)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology. (Growth Factors)
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2001 (English)In: Mechanisms of Development, ISSN 0925-4773, E-ISSN 1872-6356, Vol. 107, no 1-2, 181-5 p.Article in journal (Refereed) Published
Abstract [en]

The intermediate filament glial fibrillary acidic protein (GFAP) constitutes the major cytoskeletal protein in astrocytes (J. Neuroimmunol. 8 (1985) 203) and is traditionally referred to as a specific marker for astrocytes. To identify early glial precursors, we created GFAPpromoter-lacZ transgenic mice, using a 1.8kb 5' fragment of human GFAP. The expression of the transgene was first detected in the neuroepithelium at embryonic day 9.5. It was further found in the ventricular zone of the developing telencephalon, in the cerebellar primordium, trigeminal ganglia, and radial glia. Later, scattered beta-gal+ cells were seen in pons, brain stem and glia limitans. The results indicate that GFAP activity is regulated in a region-specific manner during central nervous system (CNS) development and that the gene is turned on in different cell types independently.

Place, publisher, year, edition, pages
2001. Vol. 107, no 1-2, 181-5 p.
Keyword [en]
Glial fibrillary acidic protein, Promoter regions (genetics), Transgenes, Central nervous system, Growth and embryonal development, Neuroglia, Cerebral ventricles, Neocortex, Cerebellum, Transcription
National Category
Medical and Health Sciences
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URN: urn:nbn:se:uu:diva-51710DOI: 10.1016/S0925-4773(01)00460-9PubMedID: 11520676OAI: oai:DiVA.org:uu-51710DiVA: diva2:79619
Available from: 2008-10-17 Created: 2008-10-17 Last updated: 2017-12-04Bibliographically approved

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Westermark, Bengt

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