Specificity and versatility in tgf-beta signaling through Smads.

By Xin-Hua Feng, R. Derynck. Annual Review of Cell and Developmental Biology, 2005

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The basics of epithelial–mesenchymal transition (EMT): A study from a structure, dynamics, and functional perspective (2019, background): “…definite the expression of several SMAD2/3 that interacts with the transcription factors like AP‐1 and Forkhead family members, Stats, and so forth (Feng & Derynck, 2005; Shi & Massagué, 2003), as well as their association with additional transcriptional activators or repressors (Hayashi et…”
Molecular antagonism and plasticity of regulatory and inflammatory T cell programs. (2008, background): “TGF-b receptor activation induces activation and phosphorylation of Smad2 and Smad3, which then bind to Smad4 and translocate to the nucleus (Feng and Derynck, 2005).”
Protection from obesity and diabetes by blockade of TGF-β/Smad3 signaling (2011, background): “TGF-b transmits its signals via dual serine/threonine kinase receptors and transcription factors called Smads, with Smad3 serving as the principal facilitator of TGF-b signals (Feng and Derynck, 2005).”
The logic of TGFβ signaling (2006, background): “The availability of such cofactors may vary depending on the cell type, partly determining the gene responses to TGFb in each cell type [30,40].”
TGFβ in Cancer (2008, background): “These Smad partners are drawn from various families of transcription factors, such as the forkhead, homeobox, zinc-finger, bHLH, and AP1 families (Feng and Derynck, 2005; Massagué et al., 2005).”