The Functional Interaction between the Paired Domain Transcription Factor Pax8 and Smad3 Is Involved in Transforming Growth Factor-β Repression of the Sodium/Iodide Symporter Gene*
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Summary
A novel mechanism of Smad3 function in regulating thyroid cell differentiation is demonstrated by functionally antagonizing the action of the paired domain transcription factor Pax8 in TGF-β-induced down-regulation of NIS gene expression in thyroid follicular cells.
- Type
- article
- Published
- 2004-01-30
- Cited by
- 114
- References
- 44
- Access
- Open access
- OpenAlex
- https://openalex.org/W2014406863
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:32118269
Keywords
PAX8, Transcription factor, Transforming growth factor, Molecular biology, Enhancer
References
- A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding.
- Identification of Smad7, a TGFβ-inducible antagonist of TGF-β signalling
- How cells read TGF-beta signals.
- Smad regulation in TGF-beta signal transduction.
- Smad signalling network.
- Promoter characterization of the rat Na+/I- symporter gene.
- The Effects of Transforming Growth Factor-β on Growth and Differentiation of the Continuous Rat Thyroid Follicular Cell Line, FRTL-5
- Determination of functional domains of the human transcription factor PAX8 responsible for its nuclear localization and transactivating potential.
- Intrathyroidal cytokine production in thyroid disease.
- Journey of the iodide transporter NIS: from its molecular identification to its clinical role in cancer.
- Characterization of the thyroid Na+/I- symporter with an anti-COOH terminus antibody.
- Sphingomyelinase and Phospholipase A2 Regulate Type I Deiodinase Expression in FRTL-5 Cells
- Cloning and characterization of the thyroid iodide transporter
- General inhibition by transforming growth factor β1 of thyrotropin and cAMP responses in human thyroid cells in primary culture
- Pax genes and their roles in cell differentiation and development.
- Transforming Growth Factor-β Repression of Matrix Metalloproteinase-1 in Dermal Fibroblasts Involves Smad3*
- Smad2 and Smad3 positively and negatively regulate TGF beta-dependent transcription through the forkhead DNA-binding protein FAST2.
- Synergistic Cooperation between Hypoxia and Transforming Growth Factor-β Pathways on Human Vascular Endothelial Growth Factor Gene Expression*
- Transforming Growth Factor-β1 Suppresses Thyrotropin-Induced Na+/I- Symporter Messenger RNA and Protein Levels in FRTL-5 Rat Thyroid Cells
- A thyroid-specific far-upstream enhancer in the human sodium/iodide symporter gene requires Pax-8 binding and cyclic adenosine 3',5'-monophosphate response element-like sequence binding proteins for full activity and is differentially regulated in normal and thyroid cancer cells.
Cited by
- Differential interactions between Th1/Th2, Th1/Th3, and Th2/Th3 cytokines in the regulation of thyroperoxidase and dual oxidase expression, and of thyroglobulin secretion in thyrocytes in vitro.
- The miR-146b-3p/PAX8/NIS Regulatory Circuit Modulates the Differentiation Phenotype and Function of Thyroid Cells during Carcinogenesis.
- FoxP3 in papillary thyroid carcinoma induces NIS repression through activation of the TGF-β1/Smad signaling pathway
- A galectina-3 na fisiologia e no câncer de tiróide: identificação de SNPs no gene LGALS3 e estudo funcional de galectina-3 in vitro e in vivo
- New Therapies for Dedifferentiated Papillary Thyroid Cancer
- Estradiol modulates TGF-β1 expression and its signaling pathway in thyroid stromal cells.
- New Insights into FoxE1 Functions: Identification of Direct FoxE1 Targets in Thyroid Cells
- Influence of signal transducer and activator of transcription-1 signaling on thyroid morphology and function.
- Effects of the Smad4 C324Y mutation on thyroid cell proliferation
- The MH1 domain of Smad3 interacts with Pax6 and represses autoregulation of the Pax6 P1 promoter
- EGF and TGF-β1 Effects on Thyroid Function
- A complex pattern of mutations and abnormal splicing of Smad4 is present in thyroid tumours
- Effects of histone acetylation on sodium iodide symporter promoter and expression of thyroid-specific transcription factors.
- Role of Transforming Growth Factor Beta in the Regulation of Thyroid Function and Growth
- Modulation of Sodium Iodide Symporter in Thyroid Cancer
- Down-regulation of the sodium/iodide symporter explains 131I-induced thyroid stunning.
- The promoter of the human sodium/iodide symporter responds to certain phthalate plasticisers.
- Apigenin in Combination with Akt Inhibition Significantly Enhances Thyrotropin-Stimulated Radioiodide Accumulation in Thyroid Cells
- The Sodium Iodide Symporter (NIS): Regulation and Approaches to Targeting for Cancer Therapeutics
- Genome-wide analysis of Pax8 binding provides new insights into thyroid functions
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