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anti-Mouse (Murine) NFATC4 Antibodies:
anti-Human NFATC4 Antibodies:
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Human Polyclonal NFATC4 Primary Antibody for IHC (p), IHC - ABIN249616
Hoey, Sun, Williamson, Xu: Isolation of two new members of the NF-AT gene family and functional characterization of the NF-AT proteins. in Immunity 1995
Human Polyclonal NFATC4 Primary Antibody for IF (p), IHC (p) - ABIN1386186
Xie, Deng, Pan, Ren, Jin, Wang, Wang, Zhu, Guo, Yuan, Shang, Liu: Chronic intermittent hypoxia induces cardiac hypertrophy by impairing autophagy through the adenosine 5'-monophosphate-activated protein kinase pathway. in Archives of biochemistry and biophysics 2016
Dog (Canine) Polyclonal NFATC4 Primary Antibody for ELISA - ABIN450047
Yao, Cho, Bergen, Madden, Choi, Ma, Bode, Dong: Nuclear factor of activated T3 is a negative regulator of Ras-JNK1/2-AP-1 induced cell transformation. in Cancer research 2007
BDNF regulates the timing of neurodevelopment via a novel mechanism of extranuclear sequestration of NFATc4 in Golgi. This leads to accelerated derepression of an NFI temporal occupancy gene program in cerebellar granule cells that includes Bdnf itself, revealing an autoregulatory loop within the program driven by BDNF and NFATc4.
Ca(2+)/calcineurin (CaN)/nuclear factor of activated T-cells (NFAT) c4 axis is required for neuritin-induced Kv4.2 transcriptional expression and potentiation of IA densities in cerebellum granule neurons.
Nfatc4 expression was coordinately upregulated by top hypoxia-activated transcription factors, while NFATc4 target genes were enriched in hypoxic neural stem cells.
results indicate that NFAT is a BACE1 transcription factor. Our study suggests that inhibition of NFAT-mediated BACE1 expression may be a valuable drug target for AD therapy
our results suggest that activation of NHE1 induces hypertrophy through the activation of NFAT3/Gata4 and OPN expression
Nuclear factor of activated T cells is activated in the endothelium of retinal microvessels in diabetic mice
L-carnitine reversed the activation of NFAT3 and PPARa caused by carboplatin through altering the phosphorylation of PTEN and AMPK.
Disrupting the calcineurin-NFAT axis by either genetic or pharmacologic approaches confers resistance to the development of social stress-induced voiding and dysfunction.
The NFATc4-dependent increase in hippocampal neurogenesis after GABAA receptor stimulation is required for suppression of anxiety response.
IL-13 specifically induced NFAT3 activation through promoting its dephosphorylation in air-liquid interface cultures of tracheal epithelial cells (mTECs).
Data suggest that expression of Itpr1 (inositol 1,4,5-triphosphate receptor 1) in cerebral cortex neurons is regulated by dopamine D2 receptors; Itpr1 is up-regulated via increased binding of NFATc4 and transcription factor AP-1 to Itpr1 promoter.
these results reveal a novel PI3K-independent role for p85alpha in controlling VEGF induction during the cellular UVB response by regulating NFAT3 activity.
Over-expression of NFATc4 up-regulated collagen III, MRTF-A (a transcriptional regulator of SMA) and the NFAT-target regulator of calcineurin 1.4.
As maturing cerebellar granule neurons become more hyperpolarized, NFATc4 binding declines leading to onset of nuclear factor one temporal binding and the NFI switch program
Syndecan-4 is essential for development of concentric myocardial hypertrophy via stretch-induced activation of the calcineurin-NFAT pathway
Data observed a significant upregulation and phosphorylation of ZAP-70, protein kinase C theta;, nuclear factor of activated T cells, and glycogen synthase kinase 3beta in Tregs prepared from injury-site-draining lymph nodes.
The functional interaction between lipin 1 and the nuclear factor of activated T cells c4 (NFATc4), is described.
Phosphorylation of NFATc4 by p38 mitogen-activated protein kinases.
NFATc4 is not regulated by calcineurin and is not essential for hypertrophic growth
Identification of a noncoding RNA repressor of the nuclear factor of activated T cells (NFAT) activity.
NFATc1 knockdown strongly reduced the number and the surface area of myotubes, NFATc4 knockdown increased the surface area of myotubes and reduced the pool of reserve cells.
TBX5 deficiency-mediated downregulation of NFAT3 is crucial for the high cytokine-producing activity of T cells
These results provided evidence supporting the oncogenic potential of NFAT3 and suggested that CDK3-mediated phosphorylation of NFAT3 has an important role in skin tumorigenesis.
Data indicate that RNA interference of NFAT isoforms NFATc1, NFATc2, NFATc3 and NFATc4 regulate gene expression differentially in human retinal microvascular endothelial cells (HRMEC).
NFAT3 expression plays a role in regulating CXCR4 expression.
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.
This is the first study to provide evidence of new and differential roles for NFAT3 and SMAD3 in the osteoarthritis process in the regulation of miR-140 transcription
Expression level of PPP3R1 and GATA4, and NFATC4 genes for transcription factors did not differ in studied subgroups of patients.
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.
Dendritic spine loss and dendritic branching simplification induced by amyloid-beta peptide exposure are mimicked by constitutively active NFATC4, and abolished when NFATC4 activation is blocked by the genetically encoded inhibitor VIVIT.
Polymorphisms in the NFATc4 gene may confer certain protection or predisposition for new-onset diabetes after transplantation (NODAT).
These data suggest that the opposing transcriptional activities of FoxP1 and Nfat3 maintain cardiomyocyte homeostasis.
The expression of COX-2 was significantly associated with the expressions of transcription factors NFAT3 and c-Fos in nonsmall cell lung cancer.
an earlier unknown NFAT3/LCN2 axis that critically controls motility in breast cancer
Data show that inhibition of NFAT3 activation by shNFAT3 significantly downregulated tumor necrosis factor (TNF)-alpha induction, its receptor TNFR1, caspase 10, caspase 3, and poly (ADP-ribose) polymerase.
Polymorphism of the NFATC4 gene plays a role in the development of human cardiac hypertrophy.
NFAT3 may play a role in estrogen receptor signaling in breast cancer cells
This study demonstrates that silica was able to activate NFAT3 in an oxygen radical-dependent manner, which was required for TNF-alpha induction.
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 of nuclear factors of activated T cells also participate in the formation of this complex. The product of this gene plays a role in the inducible expression of cytokine genes in T cells, especially in the induction of the IL-2 and IL-4. Alternatively spliced transcript variants encoding different isoforms have been noted for this gene.
cytoplasmic nuclear factor of activated T-cells 4
, nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 4
, nuclear factor of activated T-cells, cytoplasmic 4-like
, T-cell transcription factor NFAT3
, nuclear factor of activated T-cells, cytoplasmic 4
, transcription complex subunit NF-ATc4
, T cell transcription factor NFAT3