Signal transduction by the TGF-beta superfamily.
By L. Attisano, Jeffrey L. Wrana. Science, 2002
598 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/ec490f73507a86c41927dcd77d9799388951bcc8
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Citations in the corpus
- TGF-β1-induced Migration of Bone Mesenchymal Stem Cells Couples Bone Resorption and Formation (2009, unknown): “It is well established that phosphorylation of R-SMADs by T β RI is the primary TGF-β signaling pathway48,49.”
- TGF‐β signaling and the fibrotic response (2004, background): “Rather, Smads are believed to assist in the formation of a functional transcriptional complex on target promoters with other transcription factors; the activity of these transcriptional complexes is then adjusted by other signal transduction cascades whose identity varies depending on the promoter o”
- The basics of epithelial–mesenchymal transition (EMT): A study from a structure, dynamics, and functional perspective (2019, background): “TGFβ regulates transcription by Smad‐dependent and independent TGFβ receptor signaling pathways (Attisano & Wrana, 2002; Long, Zuo, & Park, 2005; Van Grunsven et al., 2007).”
- Functional diversity of protein phosphatase-1, a cellular economizer and reset button. (2004, background): “Two branches of these receptor kinases can be discerned (23).”
- Epithelial-mesenchymal transition and its implications for fibrosis. (2003, background): “Smad3 activation by TGF-β family members can also activate LEF-1 in the absence of β-catenin (80).”