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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 391-407 |
| Number of pages | 17 |
| Journal | Wiley Interdisciplinary Reviews: Systems Biology and Medicine |
| Volume | 5 |
| Issue number | 4 |
| DOIs | |
| State | Published - Mar 29 2013 |
| Externally published | Yes |
Bibliographical note
KAUST Repository Item: Exported on 2020-10-01Acknowledged KAUST grant number(s): KUK-013-04
Acknowledgements: 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.
This publication acknowledges KAUST support, but has no KAUST affiliated authors.
