A Two-Step Model for Colon Adenoma Initiation and Progression Caused by APC Loss
- 1 May 2009
- Vol. 137 (4), 623-634
- https://doi.org/10.1016/j.cell.2009.02.037
Abstract
No abstract availableKeywords
This publication has 51 references indexed in Scilit:
- Rac1 Activation Controls Nuclear Localization of β-catenin during Canonical Wnt SignalingCell, 2008
- Dual Positive and Negative Regulation of Wingless Signaling by Adenomatous Polyposis ColiScience, 2008
- A target-selected Apc -mutant rat kindred enhances the modeling of familial human colon cancerProceedings of the National Academy of Sciences, 2007
- Loss of Apc allows phenotypic manifestation of the transforming properties of an endogenous K- ras oncogene in vivoProceedings of the National Academy of Sciences, 2006
- Dual roles for adenomatous polyposis coli in regulating retinoic acid biosynthesis and Wnt during ocular developmentProceedings of the National Academy of Sciences, 2006
- C-terminal-binding protein directly activates and represses Wnt transcriptional targets in DrosophilaThe EMBO Journal, 2006
- Non-traditional roles for the Adenomatous Polyposis Coli (APC) tumor suppressor proteinGene, 2005
- Prostaglandin E2 Stimulates the β-Catenin/T Cell Factor-dependent Transcription in Colon CancerJournal of Biological Chemistry, 2005
- Rac1b, a tumor associated, constitutively active Rac1 splice variant, promotes cellular transformationOncogene, 2004
- The Wnt/β-catenin pathway regulates cardiac valve formationNature, 2003