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Here the authors report a lipopolysaccharide-induced NFkappaB enhanceosome in which TonEBP is required for the recruitment of p300 (show NOTCH1 Proteins). Increased expression of TonEBP enhances the NFkappaB activity and reduced TonEBP expression lowers it.
Data suggest that protease 2A of CVB3 exhibits substrate specificity that includes human/mouse Nfat5 in cardiomyocytes; Nfat5 inhibits CVB3 replication via mechanism that involves iNOS; anti-CVB3 activity of Nfat5 is impaired during CVB3 infection due to protease 2A-mediated cleavage of Nfat5. (CVB3 = Coxsackievirus 3; Nfat5 = tonicity-responsive nuclear factor of activated T-cells 5; iNOS = nitric oxide synthase type II)
NFAT5 can modulate different T-cell responses depending on stress conditions and stimulatory context.
results provide evidence that NFAT5 expression in macrophages enhances chronic arthritis by conferring apoptotic resistance to activated macrophages.
In vivo, osmotic stress up-regulates the SCTR (show SCTR Proteins) gene in the kidney cortex and medulla of wild-type mice, but does not do so in NFAT5(+/-) mice.
TonEBP suppresses adipogenesis and insulin (show INS Proteins) sensitivity by blocking epigenetic transition of PPARgamma2 (show PPARG Proteins)
TonEBP is a critical regulator of neuroinflammation and blood-brain barrier leakage in kainic acid-induced seizures.
PKC-alpha contributes to high NaCl-dependent activation of NFAT5 through ERK1/2.
these data support a novel function of the XO-NFAT5 axis in macrophage activation and TLR-induced arthritis
Suggest that biomechanical stretch is sufficient to activate NFAT5 both in native and cultured VSMCs where it regulates the expression of tenascin-C (show TNC Proteins).
In addition to finding many proteins already known to associate with NFAT5, many new ones whose function suggest novel aspects of NFAT5 regulation, interaction, and function, were also found.
The data suggest that in addition to calcium signaling and activation of inflammatory enzymes, autocrine/paracrine purinergic signaling contributes to the stimulatory effect of hyperosmotic stress on the expression of the NFAT5 gene in retinal pigment epithelial cells.
NFAT5-mediated expression of CACNA1C (show CACNA1C Proteins) is evolutionarily conserved. NFAT5-mediated CACNA1C (show CACNA1C Proteins) expression is critical for cardiac electrophysiological development and maturation.
Data suggest that protease 2A of CVB3 exhibits substrate specificity that includes human/mouse NFAT5 in cardiomyocytes; NFAT5 inhibits CVB3 replication via mechanism that involves iNOS; anti-CVB3 activity of NFAT5 is impaired during CVB3 infection due to protease 2A-mediated cleavage of NFAT5. (CVB3 = Coxsackievirus 3; NFAT5 = tonicity-responsive nuclear factor of activated T-cells 5; iNOS = nitric oxide synthase type II)
TonEBP expression correlated with canonical osmoregulatory targets TauT/SLC6A6 (show TAUT Proteins), SMIT/SLC5A3 (show SLC5A3 Proteins), and AR/AKR1B1 (show AKR1B1 Proteins), supporting in vitro findings that the inflammatory milieu during IDD (show COL9A3 Proteins) does not interfere with TonEBP osmoregulation. In summary, whereas TonEBP participates in the proinflammatory response to TNF-alpha (show TNF Proteins)
genetic variation in NFAT5 expression and function in the central nervous system may affect the regulation of systemic water balance
The hyperosmotic AR gene expression was dependent on activation of metalloproteinases, autocrine/paracrine TGF-beta (show TGFB1 Proteins) signaling, activation of p38 MAPK (show MAPK14 Proteins), ERK1/2, and PI3K (show PIK3CA Proteins) signal transduction pathways, and the transcriptional activity of NFAT5.
Conclusion. miR-20b acts as a tumor suppressor in the development of thymoma and thymoma-associated myasthenia gravis. The tumor suppressive function of miR-20b in thymoma could be due to its inhibition of NFAT signaling by repression of NFAT5 and CAMTA1 expression.
The hyperosmotic, but not the hypoxic, PlGF (show PGF Proteins) gene expression was in part mediated by NFAT5.
The product of this gene is a member of the nuclear factors of activated T cells family of transcription factors. Proteins belonging to this family play a central role in inducible gene transcription during the immune response. This protein regulates gene expression induced by osmotic stress in mammalian cells. Unlike monomeric members of this protein family, this protein exists as a homodimer and forms stable dimers with DNA elements. Multiple transcript variants encoding different isoforms have been found for this gene.
nuclear factor of activated T-cells 5
, nuclear factor of activated T-cells 5, tonicity-responsive
, nuclear factor of activated T-cells 5-like
, T-cell transcription factor NFAT5
, rel domain-containing transcription factor NFAT5
, tonicity-responsive enhancer binding protein
, NFAT-like protein 1
, TonE-binding protein
, glutamine rich protein H65
, osmotic response element-binding protein
, tonicity-responsive enhancer-binding protein