ArticleThe Journal of biological chemistry2019
Transforming growth factor-β (TGF-β)-induced up-regulation of TGF-β receptors at the cell surface amplifies the TGF-β response.
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
51 citing papers in PubMed, 78 citations in OpenAlex.
- Neutrophil Fate and Function in Gout: From Sterile Inflammation to Resolution.International journal of molecular sciences · 2026Review
- Modulating mesenchymal stromal cells chondrogenesis through TGF-β1 pre-conditioning during monolayer expansion in pellet culture and in a 3D mechanical load model.Journal of translational medicine · 2026Article
- Effect of LY2109761 on TGF-β1/TGFβRI/Smad Pathway and Hepatic Fibrosis Cysts Formation in Rats Infected with Echinococcus granulosus: an In Vitro and In Vivo Study.Acta parasitologica · 2026Article
- Secreted RCN3 acts as an early epithelial-fibroblast mediator via TGFβR1-Smad signaling in post-ALI pulmonary fibrosis.Cell communication and signaling : CCS · 2026Article
- CD4 + T lymphocyte and cytokine profiles in depressive disorders.BMC psychiatry · 2025Article
- T follicular helper 1 cells in blood potentially mirror salivary gland-infiltrating T cells in Sjögren's disease.Scientific reports · 2025Article
- ADI-270: an armored allogeneic gamma delta T cell therapy designed to target CD70-expressing solid and hematologic malignancies.Journal for immunotherapy of cancer · 2025Article
- Quercetin, Kaempferol and Capsaicin Counteract the TGF-β1-Induced Upregulation of αSMA and Collagen in Myoblasts.International journal of molecular sciences · 2025Article
- Fibrosis in PCLS: comparing TGF-β and fibrotic cocktail.Respiratory research · 2025Article
- Carnosine modulates Aβ-induced transcriptional aberrations in murine microglial cells.Current research in pharmacology and drug discovery · 2025Article
- Inactivation of Notch1-TGF-β-Smads Signaling Pathway by Atorvastatin Improves Cardiac Function and Hemodynamic Performance in Acute Myocardial Infarction Rats.Journal of vascular research · 2025Article
- Cell mediated reactions create TGF-β delivery limitations in engineered cartilage.Acta biomaterialia · 2024Article
- Microparticle Mediated Delivery of Apelin Improves Heart Function in Post Myocardial Infarction Mice.Circulation research · 2024Article
- In vitro evidence for the potential of EGFR inhibitors to decrease the TGF-β1-induced dispersal of circulating tumour cell clusters mediated by EGFR overexpression.Scientific reports · 2024Article
- Urolithin A Ameliorates the TGF Beta-Dependent Impairment of Podocytes Exposed to High Glucose.Journal of personalized medicine · 2024Article
- Non-immune factors cause prolonged myofibroblast phenotype in implanted synthetic heart valve scaffolds.Applied materials today · 2024Article
- Transforming growth factor-β receptors: versatile mechanisms of ligand activation.Acta pharmacologica Sinica · 2024Review
- Diffusion-limited cytokine signaling in T cell populations.iScience · 2024Article
- Suppression of the TGF-β signaling exacerbates degeneration of auditory neurons in kanamycin-induced ototoxicity in mice.Scientific reports · 2024Article
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Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Functional activation of the transforming growth factor-β (TGF-β) receptors (TGFBRs) is carefully regulated through integration of post-translational modifications, spatial regulation at the cellular level, and TGFBR availability at the cell surface. Although the bulk of TGFBRs resides inside the cells, AKT Ser/Thr kinase (AKT) activation in response to insulin or other growth factors rapidly induces transport of TGFBRs to the cell surface, thereby increasing the cell's responsiveness to TGF-β. We now demonstrate that TGF-β itself induces a rapid translocation of its own receptors to the cell surface and thus amplifies its own response. This mechanism of response amplification, which hitherto has not been reported for other cell-surface receptors, depended on AKT activation and TGF-β type I receptor kinase. In addition to an increase in cell-surface TGFBR levels, TGF-β treatment promoted TGFBR internalization, suggesting an overall amplification of TGFBR cycling. The TGF-β-induced increase in receptor presentation at the cell surface amplified TGF-β-induced SMAD family member (SMAD) activation and gene expression. Furthermore, bone morphogenetic protein 4 (BMP-4), which also induces AKT activation, increased TGFBR levels at the cell surface, leading to enhanced autocrine activation of TGF-β-responsive SMADs and gene expression, providing context for the activation of TGF-β signaling in response to BMP during development. In summary, our results indicate that TGF-β- and BMP-induced activation of low levels of cell surface-associated TGFBRs rapidly mobilizes additional TGFBRs from intracellular stores to the cell surface, increasing the abundance of cell-surface TGFBRs and cells' responsiveness to TGF-β signaling.
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.