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data suggest that NFAT1 may limit the hyperactivation of the NF-kappaB (zeige NFKB1 Proteine)-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 (zeige CD4 Proteine)(+) T cell exhaustion.
These results demonstrate a repressor role for NFAT1 in cell cycle progression and Cyclin E (zeige CCNE1 Proteine) expression in B lymphocytes, and suggest a potential function for NFAT1 protein in B cell malignancies.
Overexpression of either ca-Nfatc2 or ca-Nfatc1 (zeige NFATC1 Proteine) in mouse islets enhanced insulin (zeige INS Proteine) secretion, whereas only ca-Nfatc2 was able to promote b-cell proliferation, suggesting distinct molecular pathways mediating insulin (zeige INS Proteine) secretion vs. b-cell proliferation are regulated by NFAT (zeige NFATC1 Proteine)
our results suggest the NFAT1 plays a pivotal role as a genetic switch in CD4 (zeige CD4 Proteine)(+)/CD8 (zeige CD8A Proteine)(+) 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 (zeige HSF1 Proteine)-mediated maintenance of whole body homeostasis
NFAT (zeige NFATC1 Proteine) directs signaling enzymes to gene promoters in islets.
FOXP3 (zeige FOXP3 Proteine) can inhibit NFAT (zeige NFATC1 Proteine) driven expression of CD40L (zeige CD40LG Proteine) and IL-17 (zeige IL17A Proteine) in CD4 (zeige CD4 Proteine) 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 (zeige TLR4 Proteine) activation with the translocation of NFAT1 into mitochondria to control the microglial activation during brain infection.
Our data have shown for the first time the regulation of CacyBP/SIP (zeige CACYBP Proteine) gene expression by NFAT1. Since NFAT (zeige NFATC1 Proteine) transcription factors are involved in processes related to immune response, these results indicate potential involvement of CacyBP/SIP (zeige CACYBP Proteine) in the immune system.
An interaction of NFAT1 and the beta-catenin (zeige CTNNB1 Proteine) pathway, validate lysophosphatidic acid as an in vivo activator of beta-catenin (zeige CTNNB1 Proteine)-dependent transcription during allograft fibrogenesis.
the expression of NFATc2 promotes melanoma dedifferentiation and immune escape
NFAT1 is stimulated by subplasmalemmal Ca2 (zeige CA2 Proteine)+ microdomains, whereas NFAT4 (zeige NFATC3 Proteine) additionally requires Ca2 (zeige CA2 Proteine)+ 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 (zeige NFATC1 Proteine)-associated proteins, half of which are involved in transcriptional regulation. Among them are many hitherto unknown interaction partners of NFATc1 (zeige NFATC1 Proteine) and NFATc2 in T cells, such as Raptor (zeige RPTOR Proteine), CHEK1 (zeige CHEK1 Proteine), CREB1 (zeige CREB1 Proteine), RUNX1 (zeige RUNX1 Proteine), SATB1 (zeige SATB1 Proteine), Ikaros (zeige IKZF1 Proteine), and Helios (zeige ZNFN1A2 Proteine).
NFAT1 silencing could suppress cell migration and invasion through MMP-3 (zeige MMP3 Proteine).
FOXP1 (zeige FOXP1 Proteine) 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 fine-tunes NFATc2 and STAT3 (zeige STAT3 Proteine) transcriptional networks to integrate upstream signaling events that govern pancreatic cancer progression and growth.
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