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data suggest that NFAT1 may limit the hyperactivation of the NF-kappaB (show NFKB1 ELISA Kits)-mediated proinflammatory response in DCs and suppress autoimmunity by serving as a key regulator of DC tolerance.
These results support the idea that NFAT1 is necessary to fully suppress effector responses during Plasmodium-induced CD4 (show CD4 ELISA Kits)(+) T cell exhaustion.
These results demonstrate a repressor role for NFAT1 in cell cycle progression and Cyclin E (show CCNE1 ELISA Kits) expression in B lymphocytes, and suggest a potential function for NFAT1 protein in B cell malignancies.
Overexpression of either ca-Nfatc2 or ca-Nfatc1 (show NFATC1 ELISA Kits) in mouse islets enhanced insulin (show INS ELISA Kits) secretion, whereas only ca-Nfatc2 was able to promote b-cell proliferation, suggesting distinct molecular pathways mediating insulin (show INS ELISA Kits) secretion vs. b-cell proliferation are regulated by NFAT (show NFATC1 ELISA Kits)
our results suggest the NFAT1 plays a pivotal role as a genetic switch in CD4 (show CD4 ELISA Kits)(+)/CD8 (show CD8A ELISA Kits)(+) T cell tolerance by regulating AICD process in the T cell mediated skin inflammation.
It is a non-Hsp gene, which is essential for HSF1 (show HSF1 ELISA Kits)-mediated maintenance of whole body homeostasis
NFAT (show NFATC1 ELISA Kits) directs signaling enzymes to gene promoters in islets.
FOXP3 (show FOXP3 ELISA Kits) can inhibit NFAT (show NFATC1 ELISA Kits) driven expression of CD40L (show CD40LG ELISA Kits) and IL-17 (show IL17A ELISA Kits) in CD4 (show CD4 ELISA Kits) T cells through its interaction with NFAT1 and inhibition of this interaction by a short synthetic peptide can modulate effector T cell activity
Nfatc2 and Tob1 have non-overlapping function in T cell negative regulation and tumorigenesis.
our findings reveal a new signaling pathway in microglia that couples TLR4 (show TLR4 ELISA Kits) activation with the translocation of NFAT1 into mitochondria to control the microglial activation during brain infection.
An interaction of NFAT1 and the beta-catenin (show CTNNB1 ELISA Kits) pathway, validate lysophosphatidic acid as an in vivo activator of beta-catenin (show CTNNB1 ELISA Kits)-dependent transcription during allograft fibrogenesis.
the expression of NFATc2 promotes melanoma dedifferentiation and immune escape
NFAT1 is stimulated by subplasmalemmal Ca2 (show CA2 ELISA Kits)+ microdomains, whereas NFAT4 (show NFATC3 ELISA Kits) additionally requires Ca2 (show CA2 ELISA Kits)+ mobilization from the inner nuclear envelope by nuclear InsP3 receptors.
NFAT1 overexpression is associated with Melanoma Tumor Growth and Metastasis.
revealed more than 170 NFAT (show NFATC1 ELISA Kits)-associated proteins, half of which are involved in transcriptional regulation. Among them are many hitherto unknown interaction partners of NFATc1 (show NFATC1 ELISA Kits) and NFATc2 in T cells, such as Raptor (show RPTOR ELISA Kits), CHEK1 (show CHEK1 ELISA Kits), CREB1 (show CREB1 ELISA Kits), RUNX1 (show RUNX1 ELISA Kits), SATB1 (show SATB1 ELISA Kits), Ikaros (show IKZF1 ELISA Kits), and Helios (show ZNFN1A2 ELISA Kits).
NFAT1 silencing could suppress cell migration and invasion through MMP-3 (show MMP3 ELISA Kits).
FOXP1 (show FOXP1 ELISA Kits) has protein-protein interaction with NFAT1 on DNA and enhances breast cancer cell migration by repressing NFAT1 transcriptional activity.
we describe a novel mechanism by which GSK-3beta (show GSK3b ELISA Kits) fine-tunes NFATc2 and STAT3 (show STAT3 ELISA Kits) transcriptional networks to integrate upstream signaling events that govern pancreatic cancer progression and growth.
Up-regulation of Store-operated Ca2 (show CA2 ELISA Kits)+ Entry and Nuclear Factor of Activated T Cells Promote the Acinar Phenotype of the Primary Human Salivary Gland Cells.
This gene is a member of the nuclear factor of activated T cells (NFAT) family. The product of this gene is a DNA-binding protein with a REL-homology region (RHR) and an NFAT-homology region (NHR). This protein is present in the cytosol and only translocates to the nucleus upon T cell receptor (TCR) stimulation, where it becomes a member of the nuclear factors of activated T cells transcription complex. This complex plays a central role in inducing gene transcription during the immune response. Alternate transcriptional splice variants encoding different isoforms have been characterized.
nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 2
, nuclear factor of activated T-cells, cytoplasmic 2-like
, NFAT pre-existing subunit
, T-cell transcription factor NFAT1
, nuclear factor of activated T-cells, cytoplasmic 2
, NFAT transcription complex, preexisting component
, T cell transcription factor NFAT1
, nuclear factor of activated T-cells, preexisting component
, preexisting nuclear factor of activated T-cells 2