β-Catenin stabilization dysregulates mesenchymal cell proliferation, motility, and invasiveness and causes aggressive fibromatosis and hyperplastic cutaneous wounds
By S. Cheon, A. Cheah, Stefanie Turley, Puviindran Nadesan, R. Poon, Hans Clevers, B. Alman. Proceedings of the National Academy of Sciences of the United States of America, 2002
330 citations recorded by the source corpus.
Subfields: Classics, Molecular Biology, Rheumatology
View Paper: https://www.semanticscholar.org/paper/b5162ee8c9dafd4c468cce17590a6e9561a7fff5
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
- W. Birchmeier
- A. D. Kohn
- Alexandra Klaus
- S. Werner
- Matthias Schäfer
- R. Moon
- Hans Clevers
- Christof Niehrs
Citations in the corpus
- Wnt signalling and its impact on development and cancer (2008, background): “Moreover, uncontrolled Wnt–β-catenin signalling that is associated with elevated β-catenin levels is also linked to aggressive fibromatosis and pulmonary fibrosi”
- Cancer as an overhealing wound: an old hypothesis revisited (2008, background): “Conversely, transgenic mice, which inducibly express a stabilized form of β-catenin in mesenchymal cells, developed hyperplastic skin wounds after injury and spontaneous aggressive fibromatosi”
- WNT and β-catenin signalling: diseases and therapies (2004, background): “WNT/β-catenin signalling seems to be activated in this proces”