Nucleic Acids Research Advance Access originally published online on August 1, 2007
Nucleic Acids Research 2007 35(15):5203-5212; doi:10.1093/nar/gkm528
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Nucleic Acids Research, 2007, Vol. 35, No. 15 5203-5212
© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Molecular Biology |
Functional interactions between the Forkhead transcription factor FOXK1 and the MADS-box protein SRF
1Faculty of Life Sciences, University of Manchester, Michael Smith Building, Oxford Road, Manchester, M13 9PT, UK and 2Medizinische Klinik II, Max-Burger-Forschungszentrum, Universitat Leipzig, Johannisallee 30, D-04103 Leipzig, Germany
*To whom correspondence should be addressed. Tel: +0044 161 275 5979; Fax: +0044 161 275 5082; Email: a.d.sharrocks{at}manchester.ac.uk
Received February 9, 2007. Revised June 11, 2007. Accepted June 26, 2007.
The combinatorial control of gene expression by the association of members of different families of transcription factors is a common theme in eukaryotic transcriptional control. The MADS-box transcription factors SRF and Mcm1 represent paradigms for such regulation through their interaction with numerous partner proteins. For example, in Saccharomyces cerevisiae, Mcm1 interacts with the forkhead transcription factor Fkh2. Here, we identify a novel interaction between SRF and the Forkhead transcription factor FOXK1 in human cells. The importance of this interaction is shown for the regulation of the SRF target genes SM
-actin and PPGB. The binding of FOXK1 to the SM
-actin and PPGB promoters requires the presence of SRF on the promoter. FOXK1 acts as a transcriptional repressor and it represses SM
-actin and PPGB expression. Thus FOXK1 represents an additional member of the growing repertoire of transcription factors that can interact with SRF and modulate the transcriptional output from SRF-regulated promoters.
The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors