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APC Proteins pp 1–12Cite as

APC and β-Catenin Degradation

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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 656))

Abstract

The adenomatous polyposis coli (APC) gene encodes a tumor suppressor that is mutated in familial adenomatous polyposis (FAP) colon cancer as well as the large majority of sporadic colorectal cancers (reviewed in ref 1, Chapter by Sansom, Kwong and Dove). Most of the mutations in APC associated with increased incidence of cancer generate a truncated form of APC.2, 3 While many studies have implicated the APC protein in the regulation of the cytoskeleton (reviewed in ref 4, Chapter by Morrison, Caldwell and Kaplan et al. ), there is also compelling evidence that APC is a key component of Wnt/β-catenin signaling (reviewed in refs. 3, 5). Consistent with this, loss of APC1 and APC2 genes in Drosophila result in elevated Wnt/β-catenin signaling.6–8 Mutations of APC in mice or zebrafish also increase the susceptibility of these animals to developing colorectal cancer with elevation of Wnt/β-catenin signaling in the tumors.9,10 In this chapter, we will focus on the role of APC as a negative regulator of the Wnt/β-catenin pathway.

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Authors and Affiliations

  1. Cellular and Developmental Biology, Natural Science Building, University of Michigan, Ann Arbor, MI

    Kenneth M. Cadigan (Associate Professor of Molecular)

  2. Molecular, Cellular and Developmental Biology Natural Science Building, University of Michigan, Ann Arbor, Michigan, USA

    Jennifer Kennell

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  1. Jennifer Kennell
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  2. Kenneth M. Cadigan
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Correspondence to Kenneth M. Cadigan .

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Editors and Affiliations

  1. Cell and Developmental Biology, College of Life Sciences, University of Dundee, Dundee, Scotland, UK

    Inke S. Näthke

  2. Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA

    Brooke M. McCartney

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Kennell, J., Cadigan, K.M. (2009). APC and β-Catenin Degradation. In: Näthke, I.S., McCartney, B.M. (eds) APC Proteins. Advances in Experimental Medicine and Biology, vol 656. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-1145-2_1

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