TGF‐β receptor‐activated p38 MAP kinase mediates Smad‐independent TGF‐β responses

By Li J. Yu, M. Hébert, Ying E. Zhang. 2002

665 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/a6ed50c557975497757930d3d95b7b95b1ab93cb

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Citations in the corpus

Transforming Growth Factor- 1 to the Bone (2005, background): “Second, studies making use of a mutant T RI defective in Smad recruitment demonstrated that TGFcould still activate MAPK signaling (58, 59).”
TGF-beta and the Smad signaling pathway support transcriptomic reprogramming during epithelial-mesenchymal cell transition. (2005, background): “This receptor (ALK5(TD)mL45) is completely inactive in terms of phosphorylating R-Smads (Figure 6A), but otherwise can elicit downstream signaling via Smad-independent pathways (Yu et al., 2002; Itoh et al., 2003).”
Non-Smad TGF-β signals (2005, background): “Mutant TGF-β type I receptors that lack the Smad-docking site fail to induce EMT but can activate endogenous p38 or JNK signalling (Yu et al., 2002; Itoh et al., 2003).”
Smad-dependent and Smad-independent pathways in TGF-β family signalling (2003, background): “In addition, mutated TGF-β type I receptors, defective in Smad activation, activate p38 MAPK signalling in response to TGF-&beta”
Induction of epithelial-mesenchymal transition in alveolar epithelial cells by transforming growth factor-beta1: potential role in idiopathic pulmonary fibrosis. (2005, background): “In addition, TGF-(cid:2) 1 can signal through Smad-independent pathways, possibly involving p38 MAPK.”
Targeted disruption of TGF-β1/Smad3 signaling protects against renal tubulointerstitial fibrosis induced by unilateral ureteral obstruction (2003, positive): “Experiments utilizing mutated forms of the TGF-β type I receptor unable to bind and activate Smad proteins have clearly shown that the Smad pathway is necessary but not sufficient for induction of EMT by TGF-β (22, 23), and that other pathways involving phosphatidylinositol 3-kinase, Rho-A and p38MA”
Signaling mechanisms of the epithelial-mesenchymal transition (2014, background): “Snail2 interacts with Notch and is essential for Notch-mediated repression of E-cadherin and β-catenin activation (126, 127).”
TGF-β and epithelial-to-mesenchymal transitions (2005, background): “Interestingly, activation of p38 MAPK by TGF-b in NMuMG cells depends on integrin-mediated cell adhesion (Bhowmick et al., 2001b), and p38 is required for TGF-b-induced EMT and apoptosis, but not growth arrest (Yu et al., 2002).”
Transforming Growth Factor (TGF)-β signaling in cardiac remodeling (2010, background): “Besides Smad-mediated transcription, TGF-β activates many non-canonical signaling pathways including Erk, JNK, p38 MAPK and small GTPase pathways [16–18].”