SPECIFICITY AND VERSATILITY IN TGF-β SIGNALING THROUGH SMADS

By Xin-Hua Feng, R. Derynck. 2005

1,752 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/bc942c80a839eef14cbe0deea4e3f8a145726c1b

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In Molecular Biology

Citations in the corpus

TGF-&bgr; signaling and epithelial–mesenchymal transition in cancer progression (2013, background): “Smads activate or repress transcription through physical interactions with high-affinity DNA-binding transcription factors, and coactivators and corepressors, at regulatory gene sequences [10,11].”
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 regulation of TGFβ signal transduction (2009, background): “Regulatory mechanisms of Smad transcriptional co-factors From the numerous Smad-transcription factor complexes and their resulting mechanisms of target gene regulation (see Table S1 in the supplementary material) (Feng and Derynck, 2005), we highlight here a few selected examples that are of demonst”
Transforming Growth Factor (TGF)-β signaling in cardiac remodeling (2010, positive): “These receptor-activated Smads (R-Smads) form complexes with the common Smad, Smad4, and translocate to the nucleus, where they activate or repress gene transcription depending on the recruitment of coactivators or corepressors into transcriptional complexes [15].”
Building strong bones: molecular regulation of the osteoblast lineage (2011, background): “BMPs, which are members of the transforming growth factor-β (TGFβ) superfamily, have essential roles in a wide range of biological processe”
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…”
The E-Cadherin and N-Cadherin Switch in Epithelial-to-Mesenchymal Transition: Signaling, Therapeutic Implications, and Challenges (2019, background): “To activate cellular responses to TGF-β signals, type 1 TGF-β receptor (TβR1) needs to be phosphorylated by type 2 TGF-β receptor [89].”
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).”