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MicroRNA-214 regulates immunity-related genes in bovine mammary epithelial cells by targeting NFATc3 and TRA
regulation of nuclear localization of NFAT is isoform-specific and dependent on nuclear export processes
NFATc3-deletion attenuated metabolism syndrome, reduced inflammatory regulators expression, inactivated NF-kappaB (p65), Caspase-3 and p38/JNK signaling pathway.
FZD5 is a receptor for SFRP2 and mediates SFRP2-induced angiogenesis via calcineurin/NFATc3 pathway in endothelial cells.
Redirected splicing of calcineurin A to the fetal isoforms in adult muscle and in differentiated C2C12 slows the timing of muscle relaxation, promotes nuclear localization of calcineurin target Nfatc3, and/or affects expression of Nfatc transcription targets.
Our study demonstrates that Orai1-Ca(2+)-calcineurin-NFATc4 signaling is an essential inflammatory pathway required for TNFalpha-induced endothelial cell activation and vascular inflammation. Therefore, Orai1 may be a potential therapeutic target for treatment of inflammatory diseases.
Both NFATc3 knock-out mice and ILK conditional-knockdown mice (cKD-ILK) display symptoms of NDI (polyuria and reduced AQP2 expression).
we found that VIP inhibits NFAT nuclear translocation in primary human pulmonary artery smooth muscle cells (PASMC). Early activation of NFATc3 in IPF patients may contribute to disease progression and the increase in VIP expression could be a protective compensatory mechanism
the transcription factor NFATC3 binds to IRF7 and functions synergistically to enhance IRF7-mediated IFN expression in Plasmacytoid dendritic cells.
Ca(2+) influx through ASIC1 mediates chronic hypoxia and ET-1-induced NFATc3 nuclear import and 2) the scaffolding protein PICK1 is necessary for NFATc3 nuclear import.
AKAP150-calcineurin signaling dyad is essential for the activation of the phosphatase and the subsequent down-regulation of Kv channel currents following myocardial infarction.
Study defines the NFAT4/ miR-324-5p/Mtfr1 axis, which participates in the regulation of mitochondrial fission and cardiomyocyte apoptosis.
Nuclear factor of activated T cells is activated in the endothelium of retinal microvessels in diabetic mice
Disrupting the calcineurin-NFAT axis by either genetic or pharmacologic approaches confers resistance to the development of social stress-induced voiding and dysfunction.
NFATc3 interacted in a SUMO-dependent manner with Trim17, an E3 ubiquitin ligase necessary for neuronal apoptosis
A calcineurin- and NFAT-dependent pathway is involved in alpha-synuclein-induced degeneration of midbrain dopaminergic neurons in a Parkinson's disease mouse model.
study demonstrates for the first time that NFATc3 is necessary for macrophage iNOS expression during sepsis, which is essential for containment of bacterial infections.
GRK5, acting in a kinase independent manner, is a facilitator of NFAT activity and part of a DNA-binding complex responsible for pathological hypertrophic gene transcription.
Low intracellular hydrogen peroxide contributes to NFATc3 activation in pulmonary arterial smooth muscle.
NGF facilitates depolarization-induced NFAT activation by stimulating PI3K/Akt signaling, inactivating GSK3beta, and thereby slowing NFATc3 export from the nucleus
Toxoplasma GRA6-dependent NFAT4 activation is required for T. gondii manipulation of host immune responses to maximize the parasite virulence in a strain-dependent manner.
this study demonistrated that NFATc3 promotes Ca(2+) -dependent MMP3 expression in astroglial cells in mice.
The NFATc3 first induced the expression of its interaction partner FosB before forming the heterodimeric NFATc3-FosB transcription factor complex, which bound the proximal AP-1 site in the TF gene promoter and activated TF expression.
NFAT1 is stimulated by subplasmalemmal Ca2+ microdomains, whereas NFAT4 additionally requires Ca2+ mobilization from the inner nuclear envelope by nuclear InsP3 receptors.
Calcineurin together with its upstream molecule, calpain 2, and its downstream effector, NFAT-c3, might contribute to the development of atrial fibrillation in patients with heart valve disease and diabetes.
two NFAT isoforms (NFAT4 and NFAT1) have shifted band-pass windows for the same receptor in the GPCR signaling pathway
Data indicate that RNA interference of NFAT isoforms NFATc1, NFATc2, NFATc3 and NFATc4 regulate gene expression differentially in human retinal microvascular endothelial cells (HRMEC).
Results show that two protein isoforms NFAT1 and NFAT4 are both cytosolic and stimulated by the same Ca2+ messenger but require distinct subcellular Ca2+ signals for activity.
Suggest nuclear NF-AT3 and NF-AT4 participates in atrial structural remodeling, and that PICP and TGF-beta1 levels may be sensitive serum biomarkers to estimate atrial structural remodeling with atrial fibrillation.
Microvesicles from tumor cells transferred TrpC5 to endothelial cells, inducing the expression of P-glycoprotein by activation of the transcription factor NFATc3 (nuclear factor of activated T cells isoform c3).
AP-1 and NFAT4 complex promotes miR-23a expression.
The closely related transcription factors NFAT1 and NFAT4 possess distinct nuclear localization dynamics in response to cell stimulation.
Data indicate that NFATc3 undergoes rapid dephosphorylation and nuclear translocation that are essentially complete within 20 min, although NFATc4 remains phosphorylated and localized to the cytosol.
Abeta-activated NFAT4 proteins were associated with astrocytic BACE1 gene expression via direct interaction with the BACE1 promoter region.
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.
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
transactivation activity and role in inducing differentiation of CD4(+)CD8(+) T cells
NFAT and thyroid transcription factor-1 have roles in regulating transcription of the surfactant protein D gene
NF-AT affects neural convergent extension.
transcriptional control of morphological and electrophysiological properties of neurons is mediated by distinct NFAT interactions
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.
cytoplasmic nuclear factor of activated T-cells 3
, nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 3
, nuclear factor of activated T-cells, cytoplasmic 3
, nuclear factor of activated T-cells, cytoplasmic 3-like
, T-cell transcription factor NFAT4
, T cell transcription factor NFAT4
, nuclear factor of activated T-cells c3 isoform IE-Xa
, nuclear factor of activated T-cell