Smad3 and NFAT cooperate to induce Foxp3 expression through its enhancer

By Y. Tone, K. Furuuchi, Yoshitsugu Kojima, M. Tykocinski, M. Greene, M. Tone. Nature Immunology, 2008

823 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/8d1a9d3b4b2c331e352c3ae5ce5325460bda82e2

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Citations in the corpus

Extrathymically generated regulatory T cells control mucosal Th2 inflammation (2012, background): “showed that CNS1, which contains binding sites for transcription factors (NFAT, Smad3 and RAR/RXR) downstream of three signalling pathways implicated in iT reg cell generatio”
Control of regulatory T cell lineage commitment and maintenance (2009, background): “Molecular Regulation of Foxp3 Gene Expression One interesting characteristic of the Foxp3 gene is the weak activity of the promoter alone, as observed in luciferase reporter assays (Kim and Leonard, 2007; Tone et al., 2008).”
Peripheral CD4 T cell differentiation regulated by networks of cytokines and transcription factors (2010, background): “the second intron of the Foxp3 gene (91).”
TGF-beta: a master of all T cell trades. (2008, neutral): “TGF-β induction of Foxp3 expression appears to be mediated by the recruitment of its downstream transcription factor Smad3 to a Foxp3 enhancer element (Tone et al., 2008).”
TGF-β Activation and Function in Immunity (2013, background): “In the setting of TCR engagement, Smad3 interacts with an enhancer region of the Foxp3 gene called CNS1 (62, 63).”
Dual functions for the endoplasmic reticulum calcium sensors STIM1 and STIM2 in T cell activation and tolerance (2008, result): “Our findings are consistent with published studies demonstrating 'cooperation' of NFAT and the signal transducer Smad3 at the Foxp3 promote”
Regulatory T Cells: Mechanisms of Differentiation and Function (2012, background): “Based on the more recent neonatal studies and experiments with luciferase reporter assays, it was proposed that TGF-β-induced Smad-mediated activation of the Foxp3 gene through binding of a conserved Smad-NFAT response element (Foxp3-CNS1) in thymocytes is essential for tTreg cell generation (99), w”
T cell receptor signaling controls Foxp3 expression via PI3K, Akt, and mTOR (2008, neutral): “, 13, 17), cooperation between TGF and CD28 was reported for the Foxp3 enhancer element at 2079 to 2198 (35).”
The mTOR kinase differentially regulates effector and regulatory T cell lineage commitment. (2009, background): “TGF-b signaling activates Smad3, which, along with TCR-induced NF-AT, contributes to the induction of Foxp3 by promoting acetylation at the Foxp3 enhancer (Tone et al., 2008).”
Development and maintenance of regulatory T cells. (2013, background): “…(Battaglia et al., 2006; Hill et al., 2008; Mucida et al., 2007; Zhou et al., 2009a), and that several signaling pathways, including those of NFAT, Smad3, and the Nr4a family, are critical for inducing Foxp3 expression (Sekiya et al., 2011; Sekiya et al., 2013; Tone et al., 2008; Xu et al., 2010).”
Differentiation of Effector CD4 T Cell Populations (2010, neutral): “Smad3 and NFAT, activated by TGF-β and TCR-mediated signaling, respectively, cooperate in Foxp3 gene remodeling and expression (89).”
CD4+T Cells: Differentiation and Functions (2012, background): “NFAT through interaction with FOXP3 promoted Th17 differentiation [89, 96].”
Regulatory T Cells and Foxp3 (2011, background): “periphery (74, 75), analysis of mice deficient in CNS1 revealed that thymic differentiation of Foxp3 cells was unaffected, whereas peripheral Foxp3 induction was severely”