ReviewCold Spring Harbor perspectives in biology2016
Posttranslational Regulation of Smads.
Review in Cold Spring Harbor perspectives in biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 89 citations in OpenAlex.
- NADBiochemistry and biophysics reports · 2026Article
- TRIM9-Mediated Degradation of SMAD4 Promotes Pyroptosis and Disruption of the Endothelial Barrier in Aortic Dissection Disease.Cardiovascular toxicology · 2026Article
- STAT3-mediated transactivation of NOVA2 promotes lung adenocarcinoma metastasis by splicing SMAD4.Oncogene · 2026Article
- The long noncoding RNA VIM-AS1 and nucleoporin Nup358/RanBP2 regulate SMAD nuclear accumulation during TGF-β signaling.Nucleic acids research · 2026Article
- Comprehensive analysis of the TGF-β signaling pathway: molecular mechanisms, disease drivers, and frontiers in clinical translation.Frontiers in immunology · 2026Review
- TGF-β in hematologic malignancies: molecular functions and clinical applications.Frontiers in immunology · 2026Review
- Extracellular Vesicles in Osteogenesis: A Comprehensive Review of Mechanisms and Therapeutic Potential for Bone Regeneration.Current issues in molecular biology · 2025Review
- Beyond Repetition: The Role of Gray Zone Alleles in the Upregulation ofInternational journal of molecular sciences · 2025Article
- Implication of protein post translational modifications in gastric cancer.Frontiers in cell and developmental biology · 2025Review
- TGF‑β/Smad signaling in chronic kidney disease: Exploring post‑translational regulatory perspectives (Review).Molecular medicine reports · 2024Review
- High glutamine increases stroke risk by inducing the endothelial-to-mesenchymal transition in moyamoya disease.MedComm · 2024Article
- Targeting SMAD-Dependent Signaling: Considerations in Epithelial and Mesenchymal Solid Tumors.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Hepatitis B virus X protein and TGF-β: partners in the carcinogenic journey of hepatocellular carcinoma.Frontiers in oncology · 2024Review
- Analysis of Smad3 in the modulation of stromal extracellular matrix proteins in corneal scarring after alkali injury.Molecular vision · 2024Article
- TGF-β in correlation with tumor progression, immunosuppression and targeted therapy in colorectal cancer.Medical oncology (Northwood, London, England) · 2023Review
- Intricacies of TGF-β signaling in Treg and Th17 cell biology.Cellular & molecular immunology · 2023Review
- Cellular mechanotransduction in health and diseases: from molecular mechanism to therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Article
- Imatinib blocks tyrosine phosphorylation of Smad4 and restores TGF-β growth-suppressive signaling in BCR-ABL1-positive leukemia.Signal transduction and targeted therapy · 2023Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor β (TGF-β) family signaling dictates highly complex programs of gene expression responses, which are extensively regulated at multiple levels and vary depending on the physiological context. The formation, activation, and destruction of two major functional complexes in the TGF-β signaling pathway (i.e., the TGF-β receptor complexes and the Smad complexes that act as central mediators of TGF-β signaling) are direct targets for posttranslational regulation. Dysfunction of these complexes often leads or contributes to pathogenesis in cancer and fibrosis and in cardiovascular, and autoimmune diseases. Here we discuss recent insights into the roles of posttranslational modifications in the functions of the receptor-activated Smads in the common Smad4 and inhibitory Smads, and in the control of the physiological responses to TGF-β. It is now evident that these modifications act as decisive factors in defining the intensity and versatility of TGF-β responsiveness. Thus, the characterization of posttranslational modifications of Smads not only sheds light on how TGF-β controls physiological and pathological processes but may also guide us to manipulate the TGF-β responses for therapeutic benefits.
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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.