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Hamster Polyclonal NFAT5 Primary Antibody for ChIP, GS - ABIN267152
Johnson, Shapiro, Risbud: RNA Sequencing Reveals a Role of TonEBP Transcription Factor in Regulation of Pro-inflammatory Genes in Response to Hyperosmolarity in Healthy Nucleus Pulposus Cells: A HOMEOSTATIC RESPONSE? in The Journal of biological chemistry 2016
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results uncover an NFAT5-regulated mechanism that maintains CIITA and MHCII expression in macrophages and thus modulates their T lymphocyte priming capacity.
TonEBP haplo-deficiency is associated with dramatically reduced expression of the proinflammatory genes as well as migration in macrophages.
Data indicate a role of nuclear factor of activated T-cell 5 (NFAT5) in the development of melanoma and as a marker of cell migration, metastasis, and a therapeutic target in melanoma.
These results indicate that (i) RNF183 is predominantly expressed in the normal renal medulla, (ii) NFAT5 stimulates transcriptional activation of Rnf183 by binding to its cognate binding motif in the Rnf183 promoter, and (iii) RNF183 protects renal medullary cells from hypertonicity-induced apoptosis.
These findings suggest that TonEBP haploinsufficiency suppresses diabetes-associated hepatic steatosis and neuroinflammation.
our results suggest that increases in extracellular osmolarity and TonEBP do not play a role in controlling autophagy in NP cells.
TonEBP suppresses M2 phenotype via downregulation of the IL-10 in M1 macrophages.
Here the authors report a lipopolysaccharide-induced NFkappaB enhanceosome in which TonEBP is required for the recruitment of p300. 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)
predominant role in promoting proinflammatory macrophage functions
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 gene in the kidney cortex and medulla of wild-type mice, but does not do so in NFAT5(+/-) mice.
TonEBP suppresses adipogenesis and insulin sensitivity by blocking epigenetic transition of PPARgamma2
TonEBP is a critical regulator of neuroinflammation and blood-brain barrier leakage in kainic acid-induced seizures.
role in sodium-induced increase in monocytic cell adhesion
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.
Together, these results clearly demonstrated that hyperglycemia-induced TonEBP plays a crucial role in increasing aldose reductase and PKCdelta levels and leading to apoptotic death.
In summary, in a highly homogeneous cohort of healthy individuals withminimal confounders, gene variants in TonEBP are associated with inflammation, renal function, and BP.
NFAT5-knockout mouse FLSs also showed decreased expressions of TF and CCL2.
NFAT5 inhibits invasion and promotes apoptosis in hepatocellular carcinoma associated with osmolality
NFAT5 expression is a useful prognostic biomarker for non-small cell lung cancer patients who underwent surgical resection.
Results show that higher levels of NFAT5 expression predict a good prognosis in patients with hepatocellular carcinoma (HCC), suggesting that NFAT5 is a potential tumor-suppressing gene, and verify that NFAT5 promotes hepatoma cell apoptosis and inhibits cell growth in vitro. Also, HBV inhibits NFAT5 expression by inducing hypermethylation of the AP1-binding site in the NFAT5 promoter.
the NFAT5 pathway was involved in the regulation of biomechanical stretch-induced human arterial smooth muscle cell (HUASMC) proliferation, inflammation, and migration. Stretch promoted the expression of NFAT5 in human arterial smooth muscle cells and regulated through activation of c-Jun N-terminal kinase under these conditions
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 is evolutionarily conserved. NFAT5-mediated CACNA1C 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, SMIT/SLC5A3, and AR/AKR1B1, supporting in vitro findings that the inflammatory milieu during IDD does not interfere with TonEBP osmoregulation. In summary, whereas TonEBP participates in the proinflammatory response to TNF-alpha
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 signaling, activation of p38 MAPK, ERK1/2, and PI3K 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 gene expression was in part mediated by NFAT5.
Proteins associated with and binding NH2-terminal region of NFAT5.NUP160 and NUP205 contribute to regulation of NFAT5 transcriptional activity
Our data demonstrates the involvement of TonEBP in the mechanisms responsible for osmoadaptation to hyperosmolar stress in retinal pigment epithelium cells.
Additionally, in peritoneal dialysis the cells of the peritoneal cavity are repeatedly exposed to a rise and fall in osmotic concentrations. Here we review the current information about NFAT5 in uremic patients and patients on peritoneal dialysis.
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