ArticleThe Journal of biological chemistry2011
Non-Smad transforming growth factor-β signaling regulated by focal adhesion kinase binding the p85 subunit of phosphatidylinositol 3-kinase.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
31 citing papers in PubMed, 49 citations in OpenAlex.
- Integrated spatial and single-cell transcriptomics reveal PAK kinase as a therapeutic target in fibroblastic foci and dense fibrosis of idiopathic pulmonary fibrosis.The European respiratory journal · 2025Article
- Nf2-FAK signaling axis is critical for cranial bone ossification and regeneration.Nature communications · 2025Article
- TGFβ in malignant canine mammary tumors: relation with angiogenesis, immunologic markers and prognostic role.The veterinary quarterly · 2024Article
- HER2 phosphorylation induced by TGF-β promotes mammary morphogenesis and breast cancer progression.The Journal of cell biology · 2024Article
- A prognostic marker LTBP1 is associated with epithelial mesenchymal transition and can promote the progression of gastric cancer.Functional & integrative genomics · 2024Article
- Epithelial-Mesenchymal Transition Induced in Cancer Cells by Adhesion to Type I Collagen.International journal of molecular sciences · 2022Review
- Mitochondria in Focus: From Function to Therapeutic Strategies in Chronic Lung Diseases.Frontiers in immunology · 2021Review
- An Update on Molecular Pathways Regulating Vasculogenic Mimicry in Human Osteosarcoma and Their Role in Canine Oncology.Frontiers in veterinary science · 2021Review
- Transforming Growth Factor-β Signaling in Fibrotic Diseases and Cancer-Associated Fibroblasts.Biomolecules · 2020Review
- Article
- The Role of NLRP3 Inflammasome Activation in the Epithelial to Mesenchymal Transition Process During the Fibrosis.Frontiers in immunology · 2020Review
- B7-1 drives TGF-β stimulated pancreatic carcinoma cell migration and expression of EMT target genes.PloS one · 2019Article
- miR-542-5p Attenuates Fibroblast Activation by Targeting Integrin α6 in Silica-Induced Pulmonary Fibrosis.International journal of molecular sciences · 2018Article
- Protein kinase CK2 activation is required for transforming growth factor β-induced epithelial-mesenchymal transition.Molecular oncology · 2018Article
- TGF-β and the Tissue Microenvironment: Relevance in Fibrosis and Cancer.International journal of molecular sciences · 2018Review
- The Role of Platelet-Derived ADP and ATP in Promoting Pancreatic Cancer Cell Survival and Gemcitabine Resistance.Cancers · 2017Article
- Profibrotic up-regulation of glucose transporter 1 by TGF-β involves activation of MEK and mammalian target of rapamycin complex 2 pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Exploration of a potent PI3 kinase/mTOR inhibitor as a novel anti-fibrotic agent in IPF.Thorax · 2016Article
- Berberine inhibits Smad and non-Smad signaling cascades and enhances autophagy against pulmonary fibrosis.Journal of molecular medicine (Berlin, Germany) · 2015Article
- Transforming growth factor Beta family: insight into the role of growth factors in regulation of fracture healing biology and potential clinical applications.Mediators of inflammation · 2015Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
TGF-β modulates numerous diverse cellular phenotypes including growth arrest in epithelial cells and proliferation in fibroblasts. Although the Smad pathway is fundamental for the majority of these responses, recent evidence indicates that non-Smad pathways may also have a critical role. Here we report a novel mechanism whereby the nonreceptor tyrosine focal adhesion kinase (FAK) functions as an adaptor necessary for cell type-specific responses to TGF-β. We show that in contrast to Smad actions, non-Smad pathways, including c-Abl, PAK2, and Akt, display an obligate requirement for FAK. Interestingly, this occurs in Src null SYF cells and is independent of FAK tyrosine phosphorylation, kinase activity, and/or proline-rich sequences in the C-terminal FAT domain. FAK binds the phosphatidylinositol 3-kinase (PI3K) p85 regulatory subunit following TGF-β treatment in a subset of fibroblasts but not epithelial cells and has an obligate role in TGF-β-stimulated anchorage-independent growth and migration. Together, these results uncover a new scaffolding role for FAK as the most upstream component regulating the profibrogenic action of TGF-β and suggest that inhibiting this interaction may be useful in treating a number of fibrotic diseases.
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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 OpenQuestion graph.