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First published online September 19, 2007
doi: 10.1242/10.1242/jcs.03485


Journal of Cell Science 120, 3327-3335 (2007)
Published by The Company of Biologists 2007
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Adenomatous polyposis coli (APC): a multi-functional tumor suppressor gene

Koji Aoki and Makoto M. Taketo*

Department of Pharmacology, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan


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Fig. 1. Multiple domains and functions of APC, and its truncated mutants found in colon cancer. (A) An evolutionary tree of the fly, mouse and human APC1 and APC2 proteins drawn by a Vector NTI 7 software (Invitrogen Corporation). Note that the two fly APC genes are not direct orthologues of the two mammalian genes. (B) Schematic diagram that shows multiple domains of the full-length APC and their functions. APC stimulates cell migration through interactions with Asef, IQGAP1 or mDia. APC is involved in cell adhesion through controlling beta-catenin distribution between the nucleus/cytoplasm and the plasma membrane. APC inhibits beta-catenin/TCF transcription through interactions with beta-catenin or CtBP. APC regulates chromosome segregation through kinetochore binding, and through suppression of the canonical Wnt signalling. Red arrows and blue bars indicate `activation' and `inhibition', respectively. (C) Schematic diagram that shows one of the C-terminally truncated APC proteins and its role in tumorigenesis. Truncated APC stimulates cell migration more strongly than the full-length APC does, whereas loss of its C-terminal domains causes activation of the Wnt signalling pathway and induction of chromosome instability (CIN).

 





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