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A new twist for the tumour suppressor hamartin

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Abstract

Ezrin/radixin/moesin (ERM) proteins form crosslinks between cortical actin filaments and the plasma membrane. New findings indicate that they may also bind to the tumour-suppressor protein hamartin, thereby regulating Rho GTPases, the actin-based cytoskeleton and cell adhesion. Loss of hamartin function disrupts cell adhesion, which may contribute to the formation of tumours in individuals carrying hamartin mutations.

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Figure 1: A model for the activation of ERM proteins and hamartin, and their role in the regulation of Rho and the actin cytoskeleton.

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Authors and Affiliations

  1. the National Institute of Dental and Craniofacial Research, Oral and Pharyngeal Cancer Branch, Building 30, National Institutes of Health,, 30 Convent Drive, Bethesda, 20892–4330 , Maryland, USA

    Shigetomo Fukuhara & J. Silvio Gutkind

Authors
  1. Shigetomo Fukuhara
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  2. J. Silvio Gutkind
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Correspondence to J. Silvio Gutkind.

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Fukuhara, S., Gutkind, J. A new twist for the tumour suppressor hamartin. Nat Cell Biol 2, E76–E78 (2000). https://doi.org/10.1038/35010506

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