Published December 2012
| Version v1
Journal article
Generation of animals allowing the conditional inactivation of the Pax4 gene.
- Others:
- Department of Molecular Cell Biology [Göttingen] ; Max Planck Institute for Biophysical Chemistry (MPI-BPC) ; Max-Planck-Gesellschaft-Max-Planck-Gesellschaft
- Department of Developmental Biology ; Hagedorn Research Institute
- Génétique du développement normal et pathologique ; Université Nice Sophia Antipolis (1965 - 2019) (UNS) ; COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)
- Institut de Biologie Valrose (IBV) ; Université Nice Sophia Antipolis (1965 - 2019) (UNS) ; COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA)
- Department of Clinical Neurophysiology [Göttingen] ; Georg-August-University = Georg-August-Universität Göttingen
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.
Abstract
International audience
Additional details
- URL
- https://hal.archives-ouvertes.fr/hal-00760289
- URN
- urn:oai:HAL:hal-00760289v1
- Origin repository
- UNICA