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anti-Mouse (Murine) NFAT1 Anticorps:
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Human Monoclonal NFAT1 Primary Antibody pour ChIP, ELISA - ABIN152663
Bonnet, Rochefort, Sutendra, Archer, Haromy, Webster, Hashimoto, Bonnet, Michelakis: The nuclear factor of activated T cells in pulmonary arterial hypertension can be therapeutically targeted. dans Proceedings of the National Academy of Sciences of the United States of America 2007
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Human Polyclonal NFAT1 Primary Antibody pour DB, ELISA - ABIN548643
Dong, Patino-Lopez, Candotti, Shaw: Structure-function analysis of the WIP role in T cell receptor-stimulated NFAT activation: evidence that WIP-WASP dissociation is not required and that the WIP NH2 terminus is inhibitory. dans The Journal of biological chemistry 2007
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Cow (Bovine) Polyclonal NFAT1 Primary Antibody pour WB - ABIN2779960
Glud, Sørensen, Andrulis, Wang, Kondo, Jessen, Krenacs, Stelkovics, Wabl, Serfling, Palmetshofer, Pedersen: A tumor-suppressor function for NFATc3 in T-cell lymphomagenesis by murine leukemia virus. dans Blood 2005
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Human Polyclonal NFAT1 Primary Antibody pour IHC, IHC (p) - ABIN4339296
Quang, Leboucher, Passaro, Fuhrmann, Nourieh, Vincent-Salomon, Ghysdael: The calcineurin/NFAT pathway is activated in diagnostic breast cancer cases and is essential to survival and metastasis of mammary cancer cells. dans Cell death & disease 2015
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Human Polyclonal NFAT1 Primary Antibody pour ELISA, IHC - ABIN4339294
Celil Aydemir, Lee, Won Kim, Gardner, Prince, Mok Ahn, Lee, Young-In Lee: Nuclear factor of activated T cell mediates proinflammatory gene expression in response to mechanotransduction. dans Annals of the New York Academy of Sciences 2007
Human Polyclonal NFAT1 Primary Antibody pour ICC, IF - ABIN4339295
Perotti, Baldassari, Molla, Vegetti, Bersani, Maurichi, Santinami, Anichini, Mortarini: NFATc2 is an intrinsic regulator of melanoma dedifferentiation. dans Oncogene 2016
Human Polyclonal NFAT1 Primary Antibody pour ELISA, WB - ABIN5519044
Bai, Li, Wang, Lian, Wang: The protective effects of PCPA against monocrotaline-induced pulmonary arterial hypertension are mediated through the downregulation of NFAT-1 and NF-κB. dans International journal of molecular medicine 2018
NFATc2 isoform was the most highly expressed in murine microglia cultures, and inhibition or deletion of NFATc2 was sufficient to attenuate the ability of the microglia to secrete cytokines. AbetaPP/PS1 (Alzheimer's disease model) x NFATc2-/- mice had attenuated cytokine levels compared to AbetaPP/PS1 mice as well as reduced microgliosis and astrogliosis with no effect on plaque load.
data suggest that NFAT1 may limit the hyperactivation of the NF-kappaB-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(+) T cell exhaustion.
These results demonstrate a repressor role for NFAT1 in cell cycle progression and Cyclin E expression in B lymphocytes, and suggest a potential function for NFAT1 protein in B cell malignancies.
Overexpression of either ca-Nfatc2 or ca-Nfatc1 in mouse islets enhanced insulin secretion, whereas only ca-Nfatc2 was able to promote b-cell proliferation, suggesting distinct molecular pathways mediating insulin secretion vs. b-cell proliferation are regulated by NFAT
our results suggest the NFAT1 plays a pivotal role as a genetic switch in CD4(+)/CD8(+) 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-mediated maintenance of whole body homeostasis
NFAT directs signaling enzymes to gene promoters in islets.
FOXP3 can inhibit NFAT driven expression of CD40L and IL-17 in CD4 T cells through its interaction with NFAT1 and inhibition of this interaction by a short synthetic peptide can modulate effector T cell activity
Nuclear factor of activated T cells is activated in the endothelium of retinal microvessels in diabetic mice
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 activation with the translocation of NFAT1 into mitochondria to control the microglial activation during brain infection.
In Nfat1(-/-) CD4(+) T cells, the expression of anti-inflammatory lymphokines was mediated by NFAT2, thus directly enabling protective IL expression.
Nfatc2 activation in osteoblasts inhibits bone formation and causes cancellous bone osteopenia.
our results place NFAT-dependent mechanisms as general regulators of T-cell tolerance and show that Treg-mediated suppression of T-helper cells results from the activation of NFAT-regulated gene expression.
NFAT promotes T cell anergy and exhaustion by binding at sites that do not require cooperation with AP-1.
Ablation of NFAT1, NFAT2, or a combination of both resulted in ameliorated GvHD, due to reduced proliferation, target tissue homing, and impaired effector function of allogenic donor T cells.
our results suggest a functional cooperation between NFAT1 and JunB in mediating IL-31 gene expression in CD4(+) T cells
the NFAT1 transcription factor regulates specific functions in dendritic cells that are involved in CD4 differentiation
Because NFATc2 translocation into the nucleus occurs in an all-or-none fashion, dependent on complete dephosphorylation by calcineurin, NFATc2 controls the frequencies of cells reexpressing Il4
Our findings suggest the significance of activating NFAT1/ITGA6 signaling in aggressive NPC, defining a novel critical signaling mechanism that drives NPC invasion and metastasis and providing a novel target for future personalized therapy.
URCS with EWSR1-NFATc2 fusion share a distinct DNA methylation signature and carry characteristic copy number alterations, which emphasizes that these sarcomas should be considered separately from EwS.
NFATc2 and Sp1 seem to play a key role in the progression of pancreatic cancer.
The data indicate that expression of CRTh2 is regulated through the competitive action of GATA3 and NFAT1.
NFAT1-regulated IL6 signalling contributes to aggressive phenotypes of glioma
Results show that NFAT1 expression is regulated by ASIC2 under acidosis and that NFAT1, binds to genes clustered in pathways involved in Rho GTPase signaling and calcium signaling.
Our results indicate that NFATc2 may be used as an early diagnostic or predictive biomarker for colorectal carcinoma as well as a therapeutic target
NFATc2 enhances tumor-initiating phenotypes through the NFATc2/SOX2/ ALDH1A1 axis in lung adenocarcinoma.
NFATc2 and Sp1 are co-localized in cell nuclei and physically interact at the NFAT target sequence termed NFAT-responsive promotor construct. Sp1 increases the functional activity of its binding partner NFATc2.
Our data have shown for the first time the regulation of CacyBP/SIP gene expression by NFAT1. Since NFAT transcription factors are involved in processes related to immune response, these results indicate potential involvement of CacyBP/SIP in the immune system.
An interaction of NFAT1 and the beta-catenin pathway, validate lysophosphatidic acid as an in vivo activator of beta-catenin-dependent transcription during allograft fibrogenesis.
the expression of NFATc2 promotes melanoma dedifferentiation and immune escape
NFAT1 is stimulated by subplasmalemmal Ca2+ microdomains, whereas NFAT4 additionally requires Ca2+ 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-associated proteins, half of which are involved in transcriptional regulation. Among them are many hitherto unknown interaction partners of NFATc1 and NFATc2 in T cells, such as Raptor, CHEK1, CREB1, RUNX1, SATB1, Ikaros, and Helios.
NFAT1 silencing could suppress cell migration and invasion through MMP-3.
FOXP1 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 transcriptional networks to integrate upstream signaling events that govern pancreatic cancer progression and growth.
Up-regulation of Store-operated Ca2+ 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