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Nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 3

The product of this gene is a member of the nuclear factors of activated T cells DNA-binding transcription complex. This complex consists of at least two components: a preexisting cytosolic component that translocates to the nucleus upon T cell receptor (TCR) stimulation and an inducible nuclear component. Other members of this family participate to form this complex also. The product of this gene plays a role in the regulation of gene expression in T cells and immature thymocytes. Several transcript variants encoding distinct isoforms have been identified for this gene. [provided by RefSeq, Nov 2010] (from NCBI)
Top mentioned proteins: NFATC, CAN, V1a, NFATc4, NFAT1
Papers on NFATc3
Expression of nuclear factor of activated T cells (NFAT) and downstream muscle-specific proteins in ground squirrel skeletal and heart muscle during hibernation.
Storey et al., Ottawa, Canada. In Mol Cell Biochem, Jan 2016
NFATc3 showed an elevation in DNA-binding activity but not expression during torpor.
AKAP150 participates in calcineurin/NFAT activation during the down-regulation of voltage-gated K(+) currents in ventricular myocytes following myocardial infarction.
Scott et al., Davis, United States. In Cell Signal, Jan 2016
UNASSIGNED: The Ca(2+)-responsive phosphatase calcineurin/protein phosphatase 2B dephosphorylates the transcription factor NFATc3.
Mesenchymal Stem Cells and Cardiomyocytes Interplay to Prevent Myocardial Hypertrophy.
Lu et al., Harbin, China. In Stem Cells Transl Med, Dec 2015
Furthermore, activation of the Ca(2+)/calcineurin/nuclear factor of activated T cells cytoplasmic 3 (NFATc3) hypertrophic pathway in NRVCs was abrogated in the presence of BMSCs both in vitro and in vivo.
NFAT4-dependent miR-324-5p regulates mitochondrial morphology and cardiomyocyte cell death by targeting Mtfr1.
Li et al., Qingdao, China. In Cell Death Dis, 2014
Here we report that NFAT4, miR-324-5p and mitochondrial fission regulator 1 (Mtfr1) function in one signaling axis that regulates mitochondrial morphology and cardiomyocyte cell death.
Tanshinone IIA Prevents Leu27IGF-II-Induced Cardiomyocyte Hypertrophy Mediated by Estrogen Receptor and Subsequent Akt Activation.
Huang et al., Taiwan. In Am J Chin Med, 2014
We demonstrated that tanshinone IIA significantly enhanced Akt phosphorylation through ER activation to inhibit Leu27IGF-II-induced calcineurin expression and subsequent NFATc3 nuclear translocation to suppress myocardial hypertrophy.
Architecture and expression of the nfatc1 gene in lymphocytes.
Serfling et al., Würzburg, Germany. In Front Immunol, 2013
In lymphocytes, the three NFAT factors NFATc1 (also designated as NFAT2), NFATc2 (NFAT1), and NFATc3 (NFAT4 or NFATx) are expressed and are the targets of immune receptor signals, which lead to a rapid rise of intracellular Ca(++), the activation of phosphatase calcineurin, and to the activation of cytosolic NFATc proteins.
Cooperative roles of NF-κB and NFAT4 in polyomavirus JC regulation at the KB control element.
White et al., Philadelphia, United States. In Virology, 2012
The authors report that NFAT4 and NF-kappaB interact at the KB element to co-operatively activate both human polyomavirus JC early and late transcription and viral DNA replication.
GnRH regulation of Jun and Atf3 requires calcium, calcineurin, and NFAT.
Nilson et al., Pullman, United States. In Mol Endocrinol, 2012
Data suggest that NFAT4 is required for maximal accumulation of mRNA for proto-oncogenes c-Jun/c-Fos and Atf3 (activating transcription factor 3) in gonadotropes in response to (GnRH) gonadotropin-releasing hormone.
NFATc3 is required for chronic hypoxia-induced pulmonary hypertension in adult and neonatal mice.
Bosc et al., Albuquerque, United States. In Am J Physiol Lung Cell Mol Physiol, 2011
NFATc3 is required for chronic hypoxia-induced pulmonary hypertension in adult and neonatal mice
NFATc3 regulates the transcription of genes involved in T-cell activation and angiogenesis.
Redondo et al., Madrid, Spain. In Blood, 2011
NFATc3 is specifically required for IL2 and cyclooxygenase-2 (COX2) gene expression in T cells and for T-cell proliferation and NFATc3 regulates COX2 in endothelial cells
Opposing roles of FoxP1 and Nfat3 in transcriptional control of cardiomyocyte hypertrophy.
Kerppola et al., Ann Arbor, United States. In Mol Cell Biol, 2011
These data suggest that the opposing transcriptional activities of FoxP1 and Nfat3 maintain cardiomyocyte homeostasis.
Molecular and biophysical mechanisms of Ca2+ sparklets in smooth muscle.
Navedo et al., Seattle, United States. In J Mol Cell Cardiol, 2009
Ca(2+) sparklet activity is increased in arterial myocytes during hypertension, thus increasing Ca(2+) influx and activating the transcription factor NFATc3.
Calcineurin/NFAT signaling is required for neuregulin-regulated Schwann cell differentiation.
Crabtree et al., Stanford, United States. In Science, 2009
studies demonstrate that calcineurin and NFAT are essential for neuregulin and ErbB signaling, neural crest diversification, and differentiation of Schwann cells
The yins of T cell activation.
Liu, Baltimore, United States. In Sci Stke, 2005
Class 2 regulators include the calcipressins, which, like NFATp and NFAT4 are feedback inhibitors of calcineurin-NFAT signaling, IkappaB, and the mitogen-activated protein kinase (MAPK) phosphatases, which inhibit MAPK signaling and thus the nuclear localization of AP-1 components.
NFATc2 and NFATc3 regulate T(H)2 differentiation and modulate TCR-responsiveness of naïve T(H)cells.
Glimcher et al., Boston, United States. In Nat Immunol, 2002
We found that naïve T(H) precursors that are doubly deficient in NFATc2 and NFATc3 intrinsically differentiate into TH(2)-secreting cells, even in the absence of interleukin 4 (IL-4) production.
Signals transduced by Ca(2+)/calcineurin and NFATc3/c4 pattern the developing vasculature.
Crabtree et al., Stanford, United States. In Cell, 2001
We find that mice with disruptions of both NFATc4 and the related NFATc3 genes die around E11 with generalized defects in vessel assembly as well as excessive and disorganized growth of vessels into the neural tube and somites.
The role of NF-AT transcription factors in T cell activation and differentiation.
Avots et al., Würzburg, Germany. In Biochim Biophys Acta, 2000
The family of genuine NF-AT transcription factors consists of four members (NF-AT1 [or NF-ATp], NF-AT2 [or NF-ATc], NF-AT3 and NF-AT4 [or NF-ATx]) which are characterized by a highly conserved DNA binding domain (is designated as Rel similarity domain) and a calcineurin binding domain.
Sequential involvement of NFAT and Egr transcription factors in FasL regulation.
Glimcher et al., Boston, United States. In Immunity, 2000
The critical function of NFAT proteins in maintaining lymphoid homeostasis was revealed in mice lacking both NFATp and NFAT4 (DKO).
[Novel function of Calcineurin--multipotential factor as protein a phosphatase].
Shibasaki et al., In Nihon Rinsho, 1998
This direct binding of Calcineurin to Bcl-2 results in blockage of KFAT4 nuclear import by the prevention of Calcineurin-targetted dephosphorylation of NFAT4.
Inhibitory function of two NFAT family members in lymphoid homeostasis and Th2 development.
Glimcher et al., Boston, United States. In Immunity, 1998
Here, we show that mice lacking both NFATp and NFAT4 develop a profound lymphoproliferative disorder likely due to a lowered threshold for TCR signaling coupled with increased resistance to apoptosis secondary to defective FasL expression.
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