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Overexpression of the vimentin gene in transgenic mice inhibits normal lens cell differentiation
To investigate the role of the intermediate filament protein vimentin in the normal differentiation and morphogenesis of the eye lens fiber cells, we generated transgenic mice bearing multiple copies of the chicken vimentin gene. In most cases, the vimentin transgene was overexpressed in the lenses...
Formato: | Texto |
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Lenguaje: | English |
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The Rockefeller University Press
1989
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2115810/ https://www.ncbi.nlm.nih.gov/pubmed/2793935 |
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collection | PubMed |
description | To investigate the role of the intermediate filament protein vimentin in the normal differentiation and morphogenesis of the eye lens fiber cells, we generated transgenic mice bearing multiple copies of the chicken vimentin gene. In most cases, the vimentin transgene was overexpressed in the lenses of these animals, reaching up to 10 times the endogenous levels. This high expression of vimentin interfered very strongly with the normal differentiation of the lens fibers. The normal fiber cell denucleation and elongation processes were impaired and the animals developed pronounced cataracts, followed by extensive lens degeneration. The age of appearance and extent of these abnormalities in the different transgenic lines were directly related to the vimentin level. Electron microscopic analysis revealed that the accumulated transgenic protein forms normal intermediate filaments. |
format | Text |
id | pubmed-2115810 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1989 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21158102008-05-01 Overexpression of the vimentin gene in transgenic mice inhibits normal lens cell differentiation J Cell Biol Articles To investigate the role of the intermediate filament protein vimentin in the normal differentiation and morphogenesis of the eye lens fiber cells, we generated transgenic mice bearing multiple copies of the chicken vimentin gene. In most cases, the vimentin transgene was overexpressed in the lenses of these animals, reaching up to 10 times the endogenous levels. This high expression of vimentin interfered very strongly with the normal differentiation of the lens fibers. The normal fiber cell denucleation and elongation processes were impaired and the animals developed pronounced cataracts, followed by extensive lens degeneration. The age of appearance and extent of these abnormalities in the different transgenic lines were directly related to the vimentin level. Electron microscopic analysis revealed that the accumulated transgenic protein forms normal intermediate filaments. The Rockefeller University Press 1989-10-01 /pmc/articles/PMC2115810/ /pubmed/2793935 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Articles Overexpression of the vimentin gene in transgenic mice inhibits normal lens cell differentiation |
title | Overexpression of the vimentin gene in transgenic mice inhibits normal lens cell differentiation |
title_full | Overexpression of the vimentin gene in transgenic mice inhibits normal lens cell differentiation |
title_fullStr | Overexpression of the vimentin gene in transgenic mice inhibits normal lens cell differentiation |
title_full_unstemmed | Overexpression of the vimentin gene in transgenic mice inhibits normal lens cell differentiation |
title_short | Overexpression of the vimentin gene in transgenic mice inhibits normal lens cell differentiation |
title_sort | overexpression of the vimentin gene in transgenic mice inhibits normal lens cell differentiation |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2115810/ https://www.ncbi.nlm.nih.gov/pubmed/2793935 |