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  Neuronal co-expression of EGFP and β-galactosidase in mice causes neuropathology and premature death

Krestel, H. E., Mihaljevic, A., Hoffman, D. A., & Schneider, A. (2004). Neuronal co-expression of EGFP and β-galactosidase in mice causes neuropathology and premature death. Neurobiology of Disease, 17(2), 310-318. doi:10.1016/j.nbd.2004.05.012.

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Genre: Journal Article
Alternative Title : Neuronal co-expression of EGFP and beta-galactosidase in mice causes neuropathology and premature death

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NeurobiolDis_17_2004_310.pdf (Any fulltext), 829KB
 
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 Creators:
Krestel, Heinz Eric1, Author              
Mihaljevic, André1, Author              
Hoffman, Dax A.2, Author              
Schneider, Armin, Author
Affiliations:
1Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              
2Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497701              

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Free keywords: Cytoplasmic GFP and small beta, Greek−gal; GCSF and minocycline; Neurogenic paresis; Protein aggregates; Ubiquitin
 Abstract: Dose-dependent co-expression of enhanced green fluorescent protein (EGFP) and beta-galactosidase (beta-gal) in the cytoplasm of forebrain neurons of two independent mouse lines resulted in growth retardation, weakness, and premature lethality. In primary motor cortex and striatum, apoptosis, glial fibrillary acidic protein proliferation, and cell loss were found. In addition, we observed aggregations of EGFP and beta-gal that colocalized with ubiquitin. GFP is unlikely to be toxic per se, as a third mouse line that expressed twice as much GFP in the cytoplasm of forebrain neurons as the two affected lines was normal. Cytoplasmic aggregations of EGFP and beta-gal occurred in affected and phenotypically normal mice suggesting a storage function rather than being detrimental. We successfully prolonged survival of affected mice with granulocyte colony-stimulating factor (GCSF) and the antibiotic minocycline. These compounds could protect neurons from EGFP and beta-gal-induced dysfunction, as demise of mice started after treatment was discontinued.

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Language(s): eng - English
 Dates: 2004-01-162004-05-192004-08-072004-11-01
 Publication Status: Published in print
 Pages: 8
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Degree: -

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Title: Neurobiology of Disease
  Other : Neurobiol. Dis.
Source Genre: Journal
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Publ. Info: Oxford : Academic Press
Pages: - Volume / Issue: 17 (2) Sequence Number: - Start / End Page: 310 - 318 Identifier: ISSN: 0969-9961
CoNE: https://pure.mpg.de/cone/journals/resource/954922649144