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    Toward a quantitative understanding of the Wnt/ β -catenin pathway through simulation and experiment

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    Type
    Article
    Authors
    Lloyd-Lewis, Bethan
    Fletcher, Alexander G.
    Dale, Trevor C.
    Byrne, Helen M. cc
    KAUST Grant Number
    KUK-013-04
    Date
    2013-03-29
    Online Publication Date
    2013-03-29
    Print Publication Date
    2013-07
    Permanent link to this record
    http://hdl.handle.net/10754/600044
    
    Metadata
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    Abstract
    Wnt signaling regulates cell survival, proliferation, and differentiation throughout development and is aberrantly regulated in cancer. The pathway is activated when Wnt ligands bind to specific receptors on the cell surface, resulting in the stabilization and nuclear accumulation of the transcriptional co-activator β-catenin. Mathematical and computational models have been used to study the spatial and temporal regulation of the Wnt/β-catenin pathway and to investigate the functional impact of mutations in key components. Such models range in complexity, from time-dependent, ordinary differential equations that describe the biochemical interactions between key pathway components within a single cell, to complex, multiscale models that incorporate the role of the Wnt/β-catenin pathway target genes in tissue homeostasis and carcinogenesis. This review aims to summarize recent progress in mathematical modeling of the Wnt pathway and to highlight new biological results that could form the basis for future theoretical investigations designed to increase the utility of theoretical models of Wnt signaling in the biomedical arena. © 2013 Wiley Periodicals, Inc.
    Citation
    Lloyd-Lewis B, Fletcher AG, Dale TC, Byrne HM (2013) Toward a quantitative understanding of the Wnt/ β -catenin pathway through simulation and experiment . Wiley Interdisciplinary Reviews: Systems Biology and Medicine 5: 391–407. Available: http://dx.doi.org/10.1002/wsbm.1221.
    Sponsors
    AGF is supported by EPRSC (EP/I017909/1) and Microsoft Research, Cambridge. This publication was based on work supported in part by Award No. KUK-013-04, made by King Abdullah University of Science and Technology (KAUST). BLL was supported by Cancer Research UK. TCD was supported by Cancer Research UK, the Breast Cancer Campaign and Tenovus.
    Publisher
    Wiley
    Journal
    Wiley Interdisciplinary Reviews: Systems Biology and Medicine
    DOI
    10.1002/wsbm.1221
    PubMed ID
    23554326
    ae974a485f413a2113503eed53cd6c53
    10.1002/wsbm.1221
    Scopus Count
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