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Journal of Virology, January 2007, p. 1027-1032, Vol. 81, No. 2
0022-538X/07/$08.00+0 doi:10.1128/JVI.01699-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.
Tyrolean Cancer Research Institute at the Medical University Innsbruck, 6020 Innsbruck, Austria,1 Cell Metabolism and Differentiation Group, Institute for Biomedical Aging Research of the Austrian Academy of Sciences, 6020 Innsbruck, Austria,2 Department for Molecular and Cellular Biology, Institute for Biomedical Aging Research of the Austrian Academy of Sciences, 6020 Innsbruck, Austria3
Received 7 August 2006/ Accepted 28 October 2006
We identified the transcriptional coactivator FHL2 as a novel target of the human papillomavirus type 16 (HPV-16) E7 oncoprotein, which plays a major role in cell transformation. The interaction with FHL2 is abolished by mutations in conserved regions 1 and 2 and in the C-terminal zinc finger domain of E7, all required for its transforming potential. We found that E7 impairs the coactivator function of FHL2 on both ß-catenin/LCF-dependent and AP-1-dependent promoters. Thus, the interaction with HPV-16 E7 leads to a promoter-specific impairment of FHL2 function and this may contribute to cell transformation.
Published ahead of print on 8 November 2006.
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