Smad-dependent and Smad-independent pathways in TGF-β family signalling

By R. Derynck, Ying Zhang. Nature, 2003

4,396 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/7a027866180e8dae14604eeab6ba129f5a50dce6

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Citations in the corpus

Tumour microenvironment: TGFβ: the molecular Jekyll and Hyde of cancer (2006, neutral): “jpg" NDATA ITEM> ]> It is now generally accepted that the transforming growth factor-β ligands TGFβ1 , TGFβ2 and TGFβ3 are potent regulators of cell growth, differentiation and migratio”
Targeting TGF-β signal transduction for fibrosis and cancer therapy (2022, background): “Under different physiological and pathological conditions, different kinases or signaling pathways adjust the SMAD pathway to regulate protein expression [48].”
TGF-β signaling in fibrosis (2011, background): “In addition to Smad and MAPK, TGF-b has been shown to activate PI3 kinase/Akt, Abelson nonreceptor tyrosine kinase (c-Abl), and Rho GTPase pathways and cooperate with Wnt and Notch signaling cascades (Derynck and Zhang 2003).”
Inflammatory bone loss: pathogenesis and therapeutic intervention (2012, background): “SMADs are phosphorylated primarily after the interaction of bone morphogenetic proteins (BMPs) with their receptors, and are essential not only for activation of RUNX2 but also for other osteoblast-typical gene”
TGF-β1 Signaling and Tissue Fibrosis. (2018, background): “…coregulators of R-Smad-dependent transcription of TGF-b1 target genes such as AP-1 and Egr-1, specific negative regulators of R-Smad function such as Smad7, but also early response genes such as Nox4 and Tgfb1 itself further promote TGF-b1 signaling (Derynck and Zhang 2003; Feng and Derynck 2005).”
TGF-β and epithelial-to-mesenchymal transitions (2005, background): “Phoshorylated Smads partner with cytoplasmic Smad4 and translocate to the nucleus where Smad complexes control transcription of target genes through interaction with specific binding motifs in their gene regulatory regions (Derynck and Zhang, 2003).”
TGF-β/Smad signaling in renal fibrosis (2015, background): “Additionally, TGF-β1 is able to function through the Smad-independent pathways, including p38, ERK (Extracellular-signal-regulated kinase), MAPK, RhoGTPases, Rac, Cdc42, ILK (Integrin linked kinase) (Attisano and Wrana, 2002; Derynck and Zhang, 2003; Li et al., 2009; Loeffler andWolf, 2014).”
Reassessing epithelial to mesenchymal transition as a prerequisite for carcinoma invasion and metastasis. (2006, background): “Activation of TGF-h receptors results in signal propagation through various pathways implicated in EMT (35), including”