File:Signaling pathways regulating EMT.png
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| Description | Figure 2. Signaling pathways regulating EMT. The encounter between specific ligands and epithelial cells results in the activation of several intracellular signaling pathways that ultimately lead to the expression of core EMT-TFs such as ZEB1/2, SNAI1/2, and TWIST1 that act pleiotropically to induce EMT. These pathways are not well compartmentalized, and some overlap exists to a certain extent between them. The canonical WNT pathway is activated upon the binding of WNT ligands to the Frizzled family of membrane receptors, ensuing the release of β-catenin from the GSK3β–AXIN-APC complex. This enables its translocation to the nucleus, thereby activating TCF and LEF-1 TFs, which promotes the expression of EMT-associated genes. The NOTCH pathway is activated upon binding of DDL or JAG ligands to the NOTCH receptor, leading to the release of the active NOTCH-ICD, which translocates to the nucleus to function as a transcriptional co-activator. The Hedgehog signaling pathway is activated by members of the Hedgehog (HH) ligand family that bind to PTCH receptor and activate SMO, which recruits GLI TFs, further entailing the transcription of EMT target genes. TGFβ activates the TGFβ family of receptors that trigger the phosphorylation and activation of cytoplasmic SMAD2 and SMAD3, which further assemble with SMAD4 to migrate to the nucleus, where they activate the transcription EMT-TFs. SMAD also interacts with β-catenin and NOTCH-ICD, enabling cross-talk between the TGF-β, WNT, and NOTCH pathways. The TGFβ pathway also collaborates with the PI3K–AKT pathway, which in turn triggers the activation of the mTOR and NF-κB and the RAS–RAF–MEK–ERK signaling axis. These pathways are also triggered by the binding of several growth factors to their cognate receptors. The binding of several cytokines to their receptors triggers the phosphorylation and activation of JAKs and STATs. STAT dimers activate the transcription of genes encoding core EMT-TFs. Abbreviations: AKT: protein kinase B; AXIN: axis inhibition protein; DHH: desert hh; DLL: Delta-like; EGF: epidermal growth factor; EMT: epithelial–mesenchymal transition; ERK: extracellular signal-regulated kinase; FGF: fibroblast growth factor; GSK-3β: glycogen synthase kinase-3β; HGF: hepatocyte growth factor; IHH: Indian Hedgehog; JAG: jagged; JAK: Janus kinase; LEF-1: lymphoid enhancer binding factor 1; MAPK: mitogen-activated protein kinase; MEK: MAP kinase; mTOR: mammalian target of rapamycin; NF-κB: nuclear factor-κB; NOTCH-ICD: NOTCH receptor intracellular domain; PI3K: phosphoinositide 3-kinase; PTCH: patched; RTKs: receptor tyrosine kinases; SHH: sonic hh; SMAD: homolog of the Drosophila protein, mothers against decapentaplegic (Mad) and the Caenorhabditis elegans protein Sma; SMO: smoothened; SNAI1: snail family transcriptional repressor 1; STAT: signal transducers and activators of transcription; TβRI: TGFβ receptor type I; TβRII: TGFβ receptor type II; TCF: T cell factor; TFs: transcription factors; TGF-β: transforming growth factor-β; TWIST1: twist family BHLH transcription factor 1; VEGF: vascular endothelial growth factor; ZEB1: zinc finger E-box binding homeobox 1.Created with Biorender.com (accessed on 20 August 2023). |
| Date | |
| Source | https://www.mdpi.com/1422-0067/24/19/14481 Involvement of Epithelial-Mesenchymal Transition (EMT) in Autoimmune Diseases. Int. J. Mol. Sci. 2023, 24, 14481. https://doi.org/10.3390/ijms241914481 |
| Author | Sarrand, J.; Soyfoo, M.S. |
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© 2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
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| current | 00:11, 17 May 2024 | | 3,262 × 2,266 (588 KB) | Rasbak (talk | contribs) | {{Information |description=Figure 2. Signaling pathways regulating EMT. The encounter between specific ligands and epithelial cells results in the activation of several intracellular signaling pathways that ultimately lead to the expression of core EMT-TFs such as ZEB1/2, SNAI1/2, and TWIST1 that act pleiotropically to induce EMT. These pathways are not well compartmentalized, and some overlap exists to a certain extent between them. The canonical WNT pathway is activated upon the binding of... |
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