• Login
    JavaScript is disabled for your browser. Some features of this site may not work without it.
    Rhomboid family member 2 regulates cytoskeletal stress-associated Keratin 16. 
    •   QMRO Home
    • Blizard Institute
    • Centre for Cell Biology and Cutaneous Research
    • Rhomboid family member 2 regulates cytoskeletal stress-associated Keratin 16.
    •   QMRO Home
    • Blizard Institute
    • Centre for Cell Biology and Cutaneous Research
    • Rhomboid family member 2 regulates cytoskeletal stress-associated Keratin 16.
    ‌
    ‌

    Browse

    All of QMROCommunities & CollectionsBy Issue DateAuthorsTitlesSubjectsThis CollectionBy Issue DateAuthorsTitlesSubjects
    ‌
    ‌

    Administrators only

    Login
    ‌
    ‌

    Statistics

    Most Popular ItemsStatistics by CountryMost Popular Authors

    Rhomboid family member 2 regulates cytoskeletal stress-associated Keratin 16.

    View/Open
    Published version (2.191Mb)
    Volume
    8
    Pagination
    14174 - ?
    DOI
    10.1038/ncomms14174
    Journal
    Nat Commun
    Metadata
    Show full item record
    Abstract
    Keratin 16 (K16) is a cytoskeletal scaffolding protein highly expressed at pressure-bearing sites of the mammalian footpad. It can be induced in hyperproliferative states such as wound healing, inflammation and cancer. Here we show that the inactive rhomboid protease RHBDF2 (iRHOM2) regulates thickening of the footpad epidermis through its interaction with K16. K16 expression is absent in the thinned footpads of irhom2-/- mice compared with irhom2+/+mice, due to reduced keratinocyte proliferation. Gain-of-function mutations in iRHOM2 underlie Tylosis with oesophageal cancer (TOC), characterized by palmoplantar thickening, upregulate K16 with robust downregulation of its type II keratin binding partner, K6. By orchestrating the remodelling and turnover of K16, and uncoupling it from K6, iRHOM2 regulates the epithelial response to physical stress. These findings contribute to our understanding of the molecular mechanisms underlying hyperproliferation of the palmoplantar epidermis in both physiological and disease states, and how this 'stress' keratin is regulated.
    Authors
    Maruthappu, T; Chikh, A; Fell, B; Delaney, PJ; Brooke, MA; Levet, C; Moncada-Pazos, A; Ishida-Yamamoto, A; Blaydon, D; Waseem, A
    URI
    http://qmro.qmul.ac.uk/xmlui/handle/123456789/19007
    Collections
    • Centre for Cell Biology and Cutaneous Research [326]
    Language
    eng
    Licence information
    This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
    Copyright statements
    © The Author(s) 2017
    Twitter iconFollow QMUL on Twitter
    Twitter iconFollow QM Research
    Online on twitter
    Facebook iconLike us on Facebook
    • Site Map
    • Privacy and cookies
    • Disclaimer
    • Accessibility
    • Contacts
    • Intranet
    • Current students

    Modern Slavery Statement

    Queen Mary University of London
    Mile End Road
    London E1 4NS
    Tel: +44 (0)20 7882 5555

    © Queen Mary University of London.