Cited by 256Prion Diseases and Protein MisfoldingAlzheimer's disease research and treatmentsSkin and Cellular Biology Research

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Mice devoid of the glial fibrillary acidic protein develop normally and are susceptible to scrapie prions

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Gomi, Hiroshi, Yokoyama, Takashi, Fujimoto, Kazushi, Ikeda, Toshio, Katoh, Akira, Itoh, Takeshi, Itohara, Shigeyoshi·1995·Neuron

DOI 10.1016/0896-6273(95)90238-4

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Abstract

Glial fibrillary acidic protein (GFAP) is an intermediate filament protein specifically expressed in astrocytes in the CNS. To examine the function of GFAP in vivo, the Gfap gene was disrupted by gene targeting in embryonic stem cells. Mice homozygous for the mutation were completely devoid of GFAP but exhibited normal development and showed no obvious anatomical abnormalities in the CNS. When inoculated with infectious scrapie prions, the mutant mice exhibited neuropathological changes typical of prion diseases. Infectious prions accumulated in brains of the mutant mice to a degree similar to that in control littermates. These results suggest that GFAP is not essential for the morphogenesis of the CNS or for astrocytic responses against neuronal injury. The results argue against the hypothesis that GFAP plays a crucial role in the pathogenesis of prion diseases.

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Authors: Gomi, H., Yokoyama, T., Fujimoto, K., Ikeda, T., Katoh, A., Itoh, T., & Itohara, S.
Affiliations: Kyoto University (JP)
National Institute of Animal Health (JP)
ORCID: Yokoyama, Takashi
Fujimoto, Kazushi
Itohara, Shigeyoshi
Venue: Neuron
Publisher: Elsevier BV
Published: 1995-01
Volume: 14
Issue: 1
Pages: 29-41
ISSN: 0896-6273 (ISSN-L)
DOI: 10.1016/0896-6273(95)90238-4
OpenAlex: W2059028264
Cited by: 256
References: 67
Citations by year: 2026: 1 · 2025: 2 · 2024: 3 · 2023: 1 · 2022: 4 · 2021: 6 · 2020: 5 · 2019: 1 · 2017: 8 · 2016: 4 · 2015: 6 · 2014: 4 · 2013: 6 · 2012: 6
FWCI: 7.99
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 6772 d)
Locations: Neuron (publishedVersion)
PubMed (publishedVersion)
Funders: Japan Science and Technology Agency
Ministry of Education, Culture, Sports, Science and Technology
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Prion Diseases and Protein Misfolding
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Skin and Cellular Biology Research
Keywords: glial fibrillary acidic protein, prion disease, astrocytes, intermediate filaments, gene targeting, central nervous system development, prion accumulation, neuropathology, prion pathogenesis
MeSH terms: Animals, Astrocytes, beta-Galactosidase, Brain, Brain Chemistry, Female, Glial Fibrillary Acidic Protein, Male, Mice, Inbred C57BL, Mice, Mutant Strains, Prions, RNA, Messenger, Scrapie, Spinal Cord, Vimentin, Mutagenesis, Gene Targeting, Mice

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Mice devoid of the glial fibrillary acidic protein develop normally and are susceptible to scrapie prions

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