ArticleFrontiers in immunology2021
Latent TGF-β Activation Is a Hallmark of the Tenascin Family.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Deciphering the glioblastoma microenvironmental landscape with multi-modal radiogenomics to guide prognosis and personalized therapy.Journal of translational medicine · 2026Article
- Tenascin-C orchestrates radiotherapy-induced head and neck tumor regression.EMBO molecular medicine · 2026Article
- Intrinsic mechanisms and microenvironmental cues fine-tune plasticity of esophageal progenitors.Nature communications · 2026Article
- Novel cardiac abnormalities observed in CAH patients with tenascin-X haploinsufficiency.Frontiers in endocrinology · 2026Article
- Article
- Sustained tenascin-C expression drives neointimal hyperplasia and promotes aortocaval fistula failure.American journal of physiology. Heart and circulatory physiology · 2025Article
- ADAMTS13 attenuates renal fibrosis by suppressing thrombospondin 1 mediated TGF-β1/Smad3 activation.Toxicology and applied pharmacology · 2025Article
- Negative regulation of lymphangiogenesis by Tenascin-C delays the resolution of inflammation.iScience · 2025Article
- Harnessing the tumor microenvironment: targeted cancer therapies through modulation of epithelial-mesenchymal transition.Journal of hematology & oncology · 2025Review
- Granzyme B cleaves tenascin-C to release its C-terminal domain in rheumatoid arthritis.JCI insight · 2024Article
- Potential implications of granzyme B in keloids and hypertrophic scars through extracellular matrix remodeling and latent TGF-β activation.Frontiers in immunology · 2024Article
- Shaping Oncogenic Microenvironments: Contribution of Fibronectin.Frontiers in cell and developmental biology · 2024Review
- Extracellular matrix remodeling in tumor progression and immune escape: from mechanisms to treatments.Molecular cancer · 2023Review
- Transcriptomic analyses of joint tissues during osteoarthritis development in a rat model reveal dysregulated mechanotransduction and extracellular matrix pathways.Osteoarthritis and cartilage · 2023Article
- Biomaterials delivery strategies to repair degenerated intervertebral discs by regulating the inflammatory microenvironment.Frontiers in immunology · 2023Review
- A virological view of tenascin-C in infection.American journal of physiology. Cell physiology · 2023Review
- Tenascin-C: A Key Regulator in Angiogenesis during Wound Healing.Biomolecules · 2022Review
- COL1A1 expression induced by overexpression of both a 15‑amino acid peptide from the fibrinogen domain of tenascin‑X and integrin α11 in LX‑2 cells.Molecular medicine reports · 2022Article
- Advances on the roles of tenascin-C in cancer.Journal of cell science · 2022Article
- Tenascin-C in fibrosis in multiple organs: Translational implications.Seminars in cell & developmental biology · 2022Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor-β (TGF-β) isoforms are secreted as inactive complexes formed through non-covalent interactions between bioactive TGF-β entities and their N-terminal pro-domains called latency-associated peptides (LAP). Extracellular activation of latent TGF-β within this complex is a crucial step in the regulation of TGF-β activity for tissue homeostasis and immune cell function. We previously showed that the matrix glycoprotein Tenascin-X (TN-X) interacted with the small latent TGF-β complex and triggered the activation of the latent cytokine into a bioactive TGF-β. This activation most likely occurs through a conformational change within the latent TGF-β complex and requires the C-terminal fibrinogen-like (FBG) domain of the glycoprotein. As the FBG-like domain is highly conserved among the Tenascin family members, we hypothesized that Tenascin-C (TN-C), Tenascin-R (TN-R) and Tenascin-W (TN-W) might share with TN-X the ability to regulate TGF-β bioavailability through their C-terminal domain. Here, we demonstrate that purified recombinant full-length Tenascins associate with the small latent TGF-β complex through their FBG-like domains. This association promotes activation of the latent cytokine and subsequent TGF-β cell responses in mammary epithelial cells, such as cytostasis and epithelial-to-mesenchymal transition (EMT). Considering the pleiotropic role of TGF-β in numerous physiological and pathological contexts, our data indicate a novel common function for the Tenascin family in the regulation of tissue homeostasis under healthy and pathological conditions.
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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 OpenQuestion graph.