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Genes 2016, 7(7), 37;

Willing to Be Involved in Cancer

Medical and Biological Sciences Building, School of Biology, University of St Andrews, St Andrews KY16 9TF, UK
Medical and Biological Sciences Building, School of Medicine, University of St Andrews, St Andrews KY16 9TF, UK
Present address: Boston University School of Medicine, Silvio Conte Building, Department of Biochemistry, Boston, MA 02118, USA
Authors to whom correspondence should be addressed.
Academic Editor: Selvarangan Ponnazhagan
Received: 26 April 2016 / Revised: 4 July 2016 / Accepted: 11 July 2016 / Published: 18 July 2016
(This article belongs to the Special Issue Hippo Signaling Pathway)
Full-Text   |   PDF [2180 KB, uploaded 18 July 2016]   |  


Genome sequencing is now a common procedure, but prior to this, screening experiments using protein baits was one of the routinely used methods that, occasionally, allowed the identification of new gene products. One such experiment uncovered the gene product called willin/human Expanded/FRMD6. Initial characterization studies found that willin bound phospholipids and was strongly co-localised with actin. However, subsequently, willin was found to be the closest human sequence homologue of the Drosophila protein Expanded (Ex), sharing 60% homology with the Ex FERM domain. This in turn suggested, and then was proven that willin could activate the Hippo signalling pathway. This review describes the increasing body of knowledge about the actions of willin in a number of cellular functions related to cancer. However, like many gene products involved in aspects of cell signalling, a convincing direct role for willin in cancer remains tantalisingly elusive, at present. View Full-Text
Keywords: willin; FRMD6; FERM proteins; cancer willin; FRMD6; FERM proteins; cancer

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Gunn-Moore, F.J.; Tilston-Lünel, A.M.; Reynolds, P.A. Willing to Be Involved in Cancer. Genes 2016, 7, 37.

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