Non-Smad TGF-β signals
By A. Moustakas, C. Heldin. Journal of Cell Science, 2005
1,009 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/91be04deaf5c6a161e70148e96d17dd76fe04001
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Citations in the corpus
- Formation and function of the myofibroblast during tissue repair. (2007, background): “Alternatively, TGFb1 can regulate fibroblast gene expression independently from Smad signaling (Derynck and Zhang, 2003; Moustakas and Heldin, 2005) and expression of aSMA has been documented during the activation of Smad3-null hepatic stellate cells in culture (Schnabl et al., 2001).”
- TGFβ signalling: a complex web in cancer progression (2010, background): “In addition to Smads, which are pivotal signal transducers in TGFβ signalling, TGFβ is also known to regulate non-Smad pathways, including Erk, p38 MAPK, JUN N-terminal kinase (JNK), PI3K–Akt and small GTPase”
- Remodeling and homeostasis of the extracellular matrix: implications for fibrotic diseases and cancer (2011, background): “Autocrine TGF signaling and TGF- and SMAD3-independent mechanisms have also been implicated in fibroblast activation (Kaviratne et al., 2004; Moustakas and Heldin, 2005).”
- The basics of epithelial–mesenchymal transition (EMT): A study from a structure, dynamics, and functional perspective (2019, background): “Once activated the Smad2/3 form heterocomplexes with SMAD4 and translocation occurs into the nucleus where they regulate the cell type‐specific the expression of TGF‐β‐responsive genes (Miura et al., 2000; Moustakas & Heldin, 2005; Shi & Massagué, 2003).”
- Tumour microenvironment: TGFβ: the molecular Jekyll and Hyde of cancer (2006, neutral): “The functional TβRII–TβRI (ALK5) heteromeric signalling complex is commonly associated with human cancer, and it regulates the activation of downstream Smad-dependent and Smad-independent pathway”