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          Institute: MPI für medizinische Forschung     Collection: Abteilung Molekulare Neurobiologie     Display Documents



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ID: 226489.0, MPI für medizinische Forschung / Abteilung Molekulare Neurobiologie
Neuronal co−expression of EGFP and β−galactosidase in mice causes neuropathology and premature death
Translation of Title:Neuronal co−expression of EGFP and β−galactosidase in mice causes neuropathology and premature death
Authors:Krestel, Heinz Eric; Mihaljevic, Andre; Hoffman, Dax A.; Schneider, Armin
Language:English
Date of Publication (YYYY-MM-DD):2004-11-01
Title of Journal:Neurobiol. Dis.
Journal Abbrev.:Neurobiol. dis.
Volume:17
Issue / Number:2
Start Page:310
End Page:318
Review Status:Peer-review
Audience:Experts Only
Intended Educational Use:No
Abstract / Description:Dose−dependent co−expression of enhanced green fluorescent protein (EGFP) and small beta, Greek−galactosidase (small beta, Greek−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 small beta, Greek−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 small beta, Greek−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 small beta, Greek−gal−induced dysfunction, as demise of mice started after treatment was discontinued.
Free Keywords:Cytoplasmic GFP and small beta, Greek−gal; GCSF and minocycline; Neurogenic paresis; Protein aggregates; Ubiquitin
Last Change of the Resource (YYYY-MM-DD):--
External Publication Status:published
Document Type:Article
Version Comment:Automatic journal name synchronization
Communicated by:Wulf Kaiser
Affiliations:MPI für medizinische Forschung/Abteilung Zellphysiologie
MPI für medizinische Forschung/Abteilung Molekulare Neurobiologie
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Identifiers:DOI:10.1016%2Fj.nbd.2004.05.012
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LOCALID:6405
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