Smad-dependent and Smad-independent pathways in TGF-beta family signalling.

By R. Derynck, Ying Zhang. Nature, 2003

2,776 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/f4d22bdf74932c20a5683878bb61d0b31b208bb6

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Citations in the corpus

TGF-β and immune cells: an important regulatory axis in the tumor microenvironment and progression (2010, background): “TGFβ1 is the most commonly upregulated in tumor cells [3].”
Enamel Matrix Derivative Gel Stimulates Signal Transduction of BMP and TGF-β (2005, unknown): “Common mediator Smads (Co-Smad: Smad4) and activin receptor-like kinase (ALK) 1, which is a type I receptor and activates smads 1 and 5, are shared by BMP and TGFsignaling pathways (Miyazono, 1999; Derynck and Zhang, 2003).”
The role of TGF-β Signaling in Myocardial Infarction and Cardiac Remodeling (2007, background): “Besides Smad-mediated transcription, TGF-β activates other signaling cascades, including extracellular signalregulated kinase (Erk), c-Jun-N-terminal kinase (JNK), TGF-β-activated kinase 1 (TAK1), abelson nonreceptor tyrosine kinase (c-Abl) and p38 Mitogen-activated protein kinase (MAPK) pathways [1”
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).”
Diverse Roles of TGF-β/Smads in Renal Fibrosis and Inflammation (2011, background): “Active TGF-β then binds its receptors and functions as autocrine and paracrine manners to exert its biological and pathological activities via Smad-dependent and independent signaling pathways [5].”
Reciprocal regulation of TGF-β and reactive oxygen species: A perverse cycle for fibrosis (2015, unknown): “…studies have shown that TGF-β signaling through other non-canonical pathways, including mitogen activated protein kinase (MAPK) pathways, phosphatidylinositol-3-kinase (PI3K) pathway, and Rho-like GTPase pathways, are also critical for eliciting TGF-β 's pro ﬁ brogenic activity [25,38,50 – 61].”
Smad3 as a mediator of the fibrotic response (2004, background): “…regions between the MH1 and MH2 domains are divergent among Smads, this region contains a number of phosphorylation sites which are now appreciated to mediate the observed crosstalk between the Smad pathway and a variety of other signalling mechanisms (Lutz & Knaus 2002; Derynck & Zhang 2003).”
Transforming growth factor–β in tissue fibrosis (2020, background): “Moreover, TGF-β can also activate phosphoinositide 3-kinase/Akt and Rho GTPase pathways and cooperate with Wnt and Notch signaling cascades (Derynck and Zhang, 2003).”
TGF-β/SMAD Pathway and Its Regulation in Hepatic Fibrosis (2016, background): “SMADs also act as signal integrators and interact with other signaling pathways, such as the MAPK and NF-κB signaling pathways (Derynck and Zhang 2003; Sengupta et al. 2009).”
Aging activates adipogenic and suppresses osteogenic programs in mesenchymal marrow stroma/stem cells: the role of PPAR‐γ2 transcription factor and TGF‐β/BMP signaling pathways (2004, background): “Both TGFβ and BMP2/4 cytokines communicate with cells through Smad proteins, which serve as signal mediators between cell surface receptors and the nuclear transcriptional apparatus (Derynck & Zhang, 2003; Shi & Massague, 2003).”
TGF-beta and fibrosis in different organs - molecular pathway imprints. (2009, background): “Once released, TGF-β mediates signals through pairs of type I and type II receptors [14].”
Epithelial-mesenchymal transition and its implications for fibrosis. (2003, background): “While TGF-β is considered prototypical in its induction of EMT (50, 60, 61), there is an increase in epithelial EGF receptors in the EMT microenvironment (62), and EGF can assist in completing the conversion (50).”
Fibroblast-specific TGF-β-Smad2/3 signaling underlies cardiac fibrosis. (2017, unknown): “Activation of the TGF-β type I and II receptors also initiates noncanonical signaling that results in the activation of the MAPK cascade, which culminates in p38, JNK1/2, and ERK1/2 signaling (17).”