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. 2007 May 22;96(12):1783–1787. doi: 10.1038/sj.bjc.6603808

Figure 1.

Figure 1

A model outlining how desmosomes could contribute to tumourigenesis. Unbroken arrows indicate that plakoglobin is released from desmosomes as a result of either loss or modulation of expression of desmosomal cadherins or desmoplakin and displaces β-catenin from adherens junctions. The latter translocates to the nucleus, stimulates transcription of β-catenin-responsive genes and ultimately results in cell proliferation. Broken arrows indicate that plakoglobin liberated from desmosomes translocates to the nucleus, stimulates transcription of genes, such as c-myc or Bcl-2, and promotes uncontrolled cell growth. Further possibilities (data not shown) are that loss of expression of plakoglobin itself could predispose to cancer by reducing its ability to antagonise β-catenin-mediated Wnt signalling or that plakophilins are involved (see text). Plakoglobin (yellow), β-catenin (blue), plakophilin (red). α-cat, α-catenin; DP, desmoplakin; E-cad, E-cadherin; IFs, intermediate filaments.

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