Convergence of Wnt, beta-catenin, and cadherin pathways.

By W. Nelson, R. Nusse. Science, 2004

1,411 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/cb5e978d36bf4e057d2589dce5846b9d8e21f75a

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Citations in the corpus

The biology of CML blast crisis. (2004, background): “ences Jun signaling, thus perhaps linking these two pathways implicated in CML progression.(60,61)”
Role that phosphorylation of GSK3 plays in insulin and Wnt signalling defined by knockin analysis (2005, background): “GSK3 is a key component of the Wnt signalling pathway controlling b-catenin levels and transcriptional responses required for development and cell growth (Moon et al, 2002; Nelson and Nusse, 2004).”
Epithelial—mesenchymal and mesenchymal—epithelial transitions in carcinoma progression (2007, background): “This is often a preliminary step triggering EMT as this releases b-catenin to participate in Wnt pathway signaling (Nelson and Nusse, 2004).”
Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale. (2010, background): “Wnts are a large family of secreted proteins that are involved in many developmental processes including proliferation, differentiatation, cell migration, cell fate determination, and establishment of cell polarity (298).”
Satellite cells and the muscle stem cell niche. (2013, background): “Thus, when Wnt signaling is active, elevated levels of cytoplasmic -catenin enter the nucleus and interact with Tcf/Lef transcription factors to regulate gene expression (373).”
Tight junctions/adherens junctions: basic structure and function. (2007, background): “Moreover, growth factor-induced tyrosine phosphorylation of the cadher-in–catenin complex is associated with changes in intercellular adhesion concomitant with changes in complex composition (reviewed in Nelson and Nusse, 2004).”
Matrix Metalloproteinases, Vascular Remodeling, and Vascular Disease. (2018, background): “MMP-induced cadherin shedding promotes dissolution of adherens junctions and translocation of h-catenin to the nucleus where it acts as a transcription factor to further promote cell proliferation (Uglow et al., 2003; Nelson and Nusse, 2004).”