-Catenin degradation mediated by the CID domain of APC provides a model for the selection of APC mutations in colorectal, desmoid and duodenal tumours

By Kohler Eva Maria   Chandra Shree Harsha Vijaya   Behrens Jrgen   Schneikert Jean  

Human Molecular Genetics, Vol. 18, Iss. 2, 2009-01 ,pp. : 213-226

Oxford University Press

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APC mutations in FAP-associated desmoid tumours are non-random but not ‘just right’

By Latchford Andrew   Volikos Emmanouil   Johnson Victoria   Rogers Pauline   Suraweera Nirosha   Tomlinson Ian   Phillips Robin   Silver Andrew  

Human Molecular Genetics, Vol. 16, Iss. 1, 2007-01 ,pp. : 78-82

Oxford University Press

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The ‘just-right’ signaling model: APC somatic mutations are selected based on a specific level of activation of the  -catenin signaling cascade

By Albuquerque Cristina  

Human Molecular Genetics, Vol. 11, Iss. 13, 2002-06 ,pp. : 1549-1560

Oxford University Press

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Germline APC variants in patients with multiple colorectal adenomas, with evidence for the particular importance of E1317Q

By Lamlum Hanan  

Human Molecular Genetics, Vol. 9, Iss. 15, 2000-09 ,pp. : 2215-2221

Oxford University Press

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Truncated APC regulates the transcriptional activity of -catenin in a cell cycle dependent manner

By Schneikert Jean   Grohmann Annette   Behrens Jrgen  

Human Molecular Genetics, Vol. 16, Iss. 2, 2007-01 ,pp. : 199-209

Oxford University Press

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