ArticleBiophysical journal2009
Quantitative modeling and analysis of the transforming growth factor beta signaling pathway.
Article in Biophysical journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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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Who cites it
29 citing papers in PubMed, 63 citations in OpenAlex.
- Capturing Multiscale Dynamics of Aortic Valve Calcification with a Coupled Fluid-Structure and Systems Biology Model.ACS omega · 2026Article
- The Role of Fibroblast-Epithelial Cross-Talk on the Distribution of Distinct Fibroblast Phenotypes in the Intestinal Crypt.Bulletin of mathematical biology · 2026Article
- Optimal performance objectives in the highly conserved bone morphogenetic protein signaling pathway.NPJ systems biology and applications · 2024Article
- Computational modeling of TGF-β2:TβRI:TβRII receptor complex assembly as mediated by the TGF-β coreceptor betaglycan.Biophysical journal · 2023Article
- A novel strategy for dynamic modeling of genome-scale interaction networks.Bioinformatics (Oxford, England) · 2023Article
- Modeling Cellular Signaling Variability Based on Single-Cell Data: The TGFβ-SMAD Signaling Pathway.Methods in molecular biology (Clifton, N.J.) · 2023Review
- Data-based stochastic modeling reveals sources of activity bursts in single-cell TGF-β signaling.PLoS computational biology · 2022Article
- Mathematical model of TGF-βsignalling: feedback coupling is consistent with signal switching.BMC systems biology · 2017Article
- Deciphering Epithelial-Mesenchymal Transition Regulatory Networks in Cancer through Computational Approaches.Frontiers in oncology · 2017Review
- Population Heterogeneity in the Epithelial to Mesenchymal Transition Is Controlled by NFAT and Phosphorylated Sp1.PLoS computational biology · 2016Article
- Semi-adaptive response and noise attenuation in bone morphogenetic protein signalling.Journal of the Royal Society, Interface · 2015Article
- Transcriptional activation by NFκB increases perlecan/HSPG2 expression in the desmoplastic prostate tumor microenvironment.Journal of cellular biochemistry · 2014Article
- The self-limiting dynamics of TGF-β signaling in silico and in vitro, with negative feedback through PPM1A upregulation.PLoS computational biology · 2014Article
- Literature-based automated reconstruction, expansion, and refinement of the TGF-β superfamily ligand-receptor network.The Journal of membrane biology · 2014Article
- An integrative modeling framework reveals plasticity of TGF-β signaling.BMC systems biology · 2014Article
- Spatial aspects in the SMAD signaling pathway.Journal of mathematical biology · 2013Article
- Computational modelling of Smad-mediated negative feedback and crosstalk in the TGF-β superfamily network.Journal of the Royal Society, Interface · 2013Article
- Macrophage-specific deletion of transforming growth factor-β1 does not prevent renal fibrosis after severe ischemia-reperfusion or obstructive injury.American journal of physiology. Renal physiology · 2013Article
- A hybrid model of tumor-stromal interactions in breast cancer.Bulletin of mathematical biology · 2013Article
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Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Transforming growth factor beta (TGF-beta) signaling, which regulates multiple cellular processes including proliferation, apoptosis, and differentiation, plays an important but incompletely understood role in normal and cancerous tissues. For instance, although TGF-beta functions as a tumor suppressor in the premalignant stages of tumorigenesis, paradoxically, it also seems to act as a tumor promoter in advanced cancer leading to metastasis. The mechanisms by which TGF-beta elicits such diverse responses during cancer progression are still not entirely clear. As a first step toward understanding TGF-beta signaling quantitatively, we have developed a comprehensive, dynamic model of the canonical TGF-beta pathway via Smad transcription factors. By describing how an extracellular signal of the TGF-beta ligand is sensed by receptors and transmitted into the nucleus through intracellular Smad proteins, the model provides quantitative insight into how TGF-beta-induced responses are modulated and regulated. Subsequent model analysis shows that mechanisms associated with Smad activation by ligand-activated receptor, nuclear complex formation among Smad proteins, and inactivation of ligand-activated Smad (e.g., degradation, dephosphorylation) may be critical for regulating TGF-beta-targeted functional responses. The model was also used to predict dynamic characteristics of the Smad-mediated pathway in abnormal cells, from which we generated four testable hypotheses regarding potential mechanisms by which TGF-beta's tumor-suppressive roles may appear to morph into tumor-promotion during cancer progression.
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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.