Frost, Victoria, Grocott, Timothy ORCID: https://orcid.org/0000-0002-6321-401X, Eccles, Michael R. and Chantry, Andrew (2008) Self-regulated Pax gene expression and modulation by the TGFβ superfamily. Critical Reviews in Biochemistry and Molecular Biology, 43 (6). pp. 371-391. ISSN 1549-7798
Full text not available from this repository. (Request a copy)Abstract
The mammalian Pax gene family encode a set of paired-domain transcription factors which play essential roles in regulating proliferation, differentiation, apoptosis, cell migration, and stem-cell maintenance. Pax gene expression is necessarily tightly controlled and is associated with the demarcation of boundaries during tissue development and specification. Auto- and inter-regulation are mechanisms frequently employed to achieve precise control of Pax expression domains in a variety of tissues including the eye, central nervous system, kidney, pancreas, skeletal system, muscle, tooth, and thymus. Furthermore, aberrant Pax expression is linked to several diseases and causally associated with certain tumors. An increasing number of studies also relate patterns of Pax expression to signaling by members of the TGFß superfamily and, in some instances, this is due to disruption of Pax gene auto-regulation. Here, we review the current evidence highlighting functional and mechanistic overlap between TGFß signaling and Pax-mediated gene transcription. We conclude that self-regulation of Pax gene expression coupled with modulation by the TGFß superfamily represents a signaling axis that is frequently employed during development and disease to drive normal tissue growth, differentiation and homeostasis.
Item Type: | Article |
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Faculty \ School: | Faculty of Science > School of Biological Sciences |
UEA Research Groups: | Faculty of Science > Research Groups > Cells and Tissues |
Depositing User: | EPrints Services |
Date Deposited: | 01 Oct 2010 13:36 |
Last Modified: | 24 Sep 2024 09:31 |
URI: | https://ueaeprints.uea.ac.uk/id/eprint/293 |
DOI: | 10.1080/10409230802486208 |
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