Smad3 Protein
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Subject Areas on Research
- A mouse homologue of FAST-1 transduces TGF beta superfamily signals and is expressed during early embryogenesis.
- A phosphatase controls the fate of receptor-regulated Smads.
- Abnormal mouse lung alveolarization caused by Smad3 deficiency is a developmental antecedent of centrilobular emphysema.
- An essential role for Mad homology domain 1 in the association of Smad3 with histone deacetylase activity*.
- Axin and GSK3- control Smad3 protein stability and modulate TGF- signaling.
- Biochemical Pathways and Myometrial Cell Differentiation Leading to Nodule Formation Containing Collagen and Fibronectin.
- Biological responses to TGF-β in the mammary epithelium show a complex dependency on Smad3 gene dosage with important implications for tumor progression.
- Carcinogen 7,12-dimethylbenz[a]anthracene-induced mammary tumorigenesis is accelerated in Smad3 heterozygous mice compared to Smad3 wild type mice.
- Dopamine and α-synuclein dysfunction in Smad3 null mice.
- Essential role for Smad3 in regulating MCP-1 expression and vascular inflammation.
- Essential role of Smad3 in infarct healing and in the pathogenesis of cardiac remodeling.
- Genetic Engineering of Mesenchymal Stem Cells for Differential Matrix Deposition on 3D Woven Scaffolds.
- Impact of Smad3 loss of function on scarring and adhesion formation during tendon healing.
- Inflammatory breast cancer cells are characterized by abrogated TGFβ1-dependent cell motility and SMAD3 activity.
- Inhibition of transforming growth factor-beta/SMAD signalling by the interferon-gamma/STAT pathway.
- Ligand-dependent ubiquitination of Smad3 is regulated by casein kinase 1 gamma 2, an inhibitor of TGF-beta signaling.
- Loss of Smad3-mediated negative regulation of Runx2 activity leads to an alteration in cell fate determination.
- Loss of phosphatase and tensin homologue increases transforming growth factor beta-mediated invasion with enhanced SMAD3 transcriptional activity.
- MiR-106a-5p modulates apoptosis and metabonomics changes by TGF-β/Smad signaling pathway in cleft palate.
- Nomenclature: vertebrate mediators of TGFbeta family signals.
- Novel bone morphogenetic protein signaling through Smad2 and Smad3 to regulate cancer progression and development.
- Nox4 mediates TGF-beta1-induced retinoblastoma protein phosphorylation, proliferation, and hypertrophy in human airway smooth muscle cells.
- Overexpression of extracellular superoxide dismutase reduces acute radiation induced lung toxicity.
- PPARgamma agonists prevent TGFbeta1/Smad3-signaling in human hepatic stellate cells.
- Primary cilia and the reciprocal activation of AKT and SMAD2/3 regulate stretch-induced autophagy in trabecular meshwork cells.
- Reciprocal SOX2 regulation by SMAD1-SMAD3 is critical for anoikis resistance and metastasis in cancer.
- Role of the autotaxin-lysophosphatidic acid axis in glaucoma, aqueous humor drainage and fibrogenic activity.
- SMAD3 deficiency promotes vessel wall remodeling, collagen fiber reorganization and leukocyte infiltration in an inflammatory abdominal aortic aneurysm mouse model.
- SMAD3 promotes expression and activity of the androgen receptor in prostate cancer.
- Salmonella disrupts lymph node architecture by TLR4-mediated suppression of homeostatic chemokines.
- Ski inhibits TGF-β/phospho-Smad3 signaling and accelerates hypertrophic differentiation in chondrocytes.
- Smad3 Signaling Promotes Fibrosis While Preserving Cardiac and Aortic Geometry in Obese Diabetic Mice.
- Smad3 deficiency attenuates bleomycin-induced pulmonary fibrosis in mice.
- Smad3 has a critical role in TGF-beta-mediated growth inhibition and apoptosis in colonic epithelial cells.
- Smad3 signaling critically regulates fibroblast phenotype and function in healing myocardial infarction.
- Smad3-Smad4 and AP-1 complexes synergize in transcriptional activation of the c-Jun promoter by transforming growth factor beta.
- Smad3-dependent nuclear translocation of beta-catenin is required for TGF-beta1-induced proliferation of bone marrow-derived adult human mesenchymal stem cells.
- Smads bind directly to the Jun family of AP-1 transcription factors.
- TGF-beta-induced phosphorylation of Smad3 regulates its interaction with coactivator p300/CREB-binding protein.
- TGFβ/Smad3 signal pathway is not required for epidermal Langerhans cell development.
- Targeted disruption of Smad3 reveals an essential role in transforming growth factor beta-mediated signal transduction.
- The Smads: transcriptional regulation and mouse models.
- The loss of Smad3 results in a lower rate of bone formation and osteopenia through dysregulation of osteoblast differentiation and apoptosis.
- The role of Smad3 in mediating mouse hepatic stellate cell activation.
- The type III TGF-beta receptor signals through both Smad3 and the p38 MAP kinase pathways to contribute to inhibition of cell proliferation.
- The type III TGF-beta receptor suppresses breast cancer progression through GIPC-mediated inhibition of TGF-beta signaling.
- Transcriptional regulation of N-acetylglutamate synthase.
- Transcriptome analysis reveals autophagy as regulator of TGFβ/Smad-induced fibrogenesis in trabecular meshwork cells.
- Transforming growth factor beta 1 dysregulation in a human oral carcinoma tumour progression model.
- Transforming growth factor beta-mediated transcriptional repression of c-myc is dependent on direct binding of Smad3 to a novel repressive Smad binding element.
- Transforming growth factor beta3 regulates the versican variants in the extracellular matrix-rich uterine leiomyomas.
- Transforming growth factor β-mediated suppression of antitumor T cells requires FoxP1 transcription factor expression.
- Transforming growth factor-beta-mediated p15(INK4B) induction and growth inhibition in astrocytes is SMAD3-dependent and a pathway prominently altered in human glioma cell lines.
- Transforming growth factor-beta1 inhibition of vascular smooth muscle cell activation is mediated via Smad3.
- Tumor suppressor Smad4 is a transforming growth factor beta-inducible DNA binding protein.