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Generation of animals allowing the conditional inactivation of the Pax4 gene
Pax4 belongs to the paired-box family of transcription factors. The analysis of loss- and gain-of-function mutant animals revealed that this factor plays a crucial role in the endocrine pancreas. Indeed, Pax4 is required for the genesis of insulin-producing beta-cells. Remarkably, the sole misexpres...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Netherlands
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3505494/ https://www.ncbi.nlm.nih.gov/pubmed/22717987 http://dx.doi.org/10.1007/s11248-012-9624-0 |
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author | Kordowich, Simon Serup, Palle Collombat, Patrick Mansouri, Ahmed |
author_facet | Kordowich, Simon Serup, Palle Collombat, Patrick Mansouri, Ahmed |
author_sort | Kordowich, Simon |
collection | PubMed |
description | Pax4 belongs to the paired-box family of transcription factors. The analysis of loss- and gain-of-function mutant animals revealed that this factor plays a crucial role in the endocrine pancreas. Indeed, Pax4 is required for the genesis of insulin-producing beta-cells. Remarkably, the sole misexpression of Pax4 in glucagon-expressing cells is able to induce their regeneration, endow these with beta-cell features, and thereby counter chemically induced diabetes. However, the function of Pax4 in adult endocrine cells remains unclear. Herein, we report the generation of Pax4 conditional knockout mice that will allow the analysis of Pax4 function in mature beta-cells, as well as in the adult central nervous system. |
format | Online Article Text |
id | pubmed-3505494 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Springer Netherlands |
record_format | MEDLINE/PubMed |
spelling | pubmed-35054942012-11-28 Generation of animals allowing the conditional inactivation of the Pax4 gene Kordowich, Simon Serup, Palle Collombat, Patrick Mansouri, Ahmed Transgenic Res Original Paper Pax4 belongs to the paired-box family of transcription factors. The analysis of loss- and gain-of-function mutant animals revealed that this factor plays a crucial role in the endocrine pancreas. Indeed, Pax4 is required for the genesis of insulin-producing beta-cells. Remarkably, the sole misexpression of Pax4 in glucagon-expressing cells is able to induce their regeneration, endow these with beta-cell features, and thereby counter chemically induced diabetes. However, the function of Pax4 in adult endocrine cells remains unclear. Herein, we report the generation of Pax4 conditional knockout mice that will allow the analysis of Pax4 function in mature beta-cells, as well as in the adult central nervous system. Springer Netherlands 2012-06-21 2012 /pmc/articles/PMC3505494/ /pubmed/22717987 http://dx.doi.org/10.1007/s11248-012-9624-0 Text en © The Author(s) 2012 https://creativecommons.org/licenses/by/4.0/ This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited. |
spellingShingle | Original Paper Kordowich, Simon Serup, Palle Collombat, Patrick Mansouri, Ahmed Generation of animals allowing the conditional inactivation of the Pax4 gene |
title | Generation of animals allowing the conditional inactivation of the Pax4 gene |
title_full | Generation of animals allowing the conditional inactivation of the Pax4 gene |
title_fullStr | Generation of animals allowing the conditional inactivation of the Pax4 gene |
title_full_unstemmed | Generation of animals allowing the conditional inactivation of the Pax4 gene |
title_short | Generation of animals allowing the conditional inactivation of the Pax4 gene |
title_sort | generation of animals allowing the conditional inactivation of the pax4 gene |
topic | Original Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3505494/ https://www.ncbi.nlm.nih.gov/pubmed/22717987 http://dx.doi.org/10.1007/s11248-012-9624-0 |
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