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Nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 4

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. [provided by RefSeq, Oct 2008] (from NCBI)
Top mentioned proteins: CAN, V1a, NFATc3, NFATC, GATA4
Papers on NFATc4
Expression of nuclear factor of activated T cells (NFAT) and downstream muscle-specific proteins in ground squirrel skeletal and heart muscle during hibernation.
Storey et al., Ottawa, Canada. In Mol Cell Biochem, Jan 2016
NFATc4 increased throughout the torpor-arousal cycle in both tissues, and NFATc1 showed this trend in cardiac muscle only.
Phenylephrine promotes cardiac fibroblast proliferation through calcineurin-NFAT pathway.
Zhu et al., Nantong, China. In Front Biosci, Dec 2015
Green fluorescent protein-tagged NFAT3 was used to determine the cellular location of NFAT3.
NFATc4 Regulates Sox9 Gene Expression in Acinar Cell Plasticity and Pancreatic Cancer Initiation.
Koenig et al., Göttingen, Germany. In Stem Cells Int, Dec 2015
We show that the inflammatory transcription factor NFATc4 is highly induced and localizes in the nucleus in response to inflammation-induced EGFR signaling.
[Role of calcineurin-nuclear factor of activated T cells signaling pathway in myoblast apoptosis induced by cyclic tensile strain].
Yuan et al., In Hua Xi Kou Qiang Yi Xue Za Zhi, Oct 2015
Protein levels of NFAT3 were evaluated by Western blot.
NFAT isoforms play distinct roles in TNFα-induced retinal leukostasis.
Penn et al., Nashville, United States. In Sci Rep, 2014
This showed that NFATc1 siRNA increased ICAM1 expression, NFATc2 siRNA reduced CX3CL1, VCAM1, SELE, and ICAM1 expression, NFATc3 siRNA increased CX3CL1 and SELE expression, and NFATc4 siRNA reduced SELE expression.
Inhibition of the NFAT pathway alleviates amyloid β neurotoxicity in a mouse model of Alzheimer's disease.
Hyman et al., United States. In J Neurosci, 2012
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.
Genetic polymorphisms of the transcription factor NFATc4 and development of new-onset diabetes after transplantation in Hispanic kidney transplant recipients.
Hutchinson et al., Los Angeles, United States. In Transplantation, 2012
Polymorphisms in the NFATc4 gene may confer certain protection or predisposition for new-onset diabetes after transplantation (NODAT).
Opposing roles of FoxP1 and Nfat3 in transcriptional control of cardiomyocyte hypertrophy.
Kerppola et al., Ann Arbor, United States. In Mol Cell Biol, 2011
These data suggest that the opposing transcriptional activities of FoxP1 and Nfat3 maintain cardiomyocyte homeostasis.
Interrelationship between cardiac hypertrophy, heart failure, and chronic kidney disease: endoplasmic reticulum stress as a mediator of pathogenesis.
Austin et al., Hamilton, Canada. In Circ Res, 2011
Sarcoplasmic reticulum/ER Ca2+ disequilibrium can lead to cardiac hypertrophy via cytosolic Ca2+ elevation and stimulation of the Ca2+/calmodulin, calcineurin, NF-AT3 pathway.
Syndecan-4 is essential for development of concentric myocardial hypertrophy via stretch-induced activation of the calcineurin-NFAT pathway.
Christensen et al., Oslo, Norway. In Plos One, 2010
Syndecan-4 is essential for development of concentric myocardial hypertrophy via stretch-induced activation of the calcineurin-NFAT pathway
[Expression and significance of COX-2 and its transcription factors NFAT3 and c-Jun in non-small cell lung cancer].
He et al., Beijing, China. In Zhongguo Fei Ai Za Zhi, 2010
The expression of COX-2 was significantly associated with the expressions of transcription factors NFAT3 and c-Fos in nonsmall cell lung cancer.
Patient-specific induced pluripotent stem-cell-derived models of LEOPARD syndrome.
Lemischka et al., New York City, United States. In Nature, 2010
We show that in vitro-derived cardiomyocytes from LEOPARD syndrome iPSCs are larger, have a higher degree of sarcomeric organization and preferential localization of NFATC4 in the nucleus when compared with cardiomyocytes derived from human embryonic stem cells or wild-type iPSCs derived from a healthy brother of one of the LEOPARD syndrome patients.
Calcineurin/NFAT signaling is required for neuregulin-regulated Schwann cell differentiation.
Crabtree et al., Stanford, United States. In Science, 2009
studies demonstrate that calcineurin and NFAT are essential for neuregulin and ErbB signaling, neural crest diversification, and differentiation of Schwann cells
Transcription factor NFAT, its role in cancer development, and as a potential target for chemoprevention.
Huan et al., New York City, United States. In Curr Cancer Drug Targets, 2007
Experimental evidence accumulated from our studies indicate the critical role of NFAT3 in some carcinogen-induced cell transformation and tumorigenicity.
Neurotrophins and netrins require calcineurin/NFAT signaling to stimulate outgrowth of embryonic axons.
Crabtree et al., Stanford, United States. In Cell, 2003
Neurotrophins and netrins stimulate calcineurin-dependent nuclear localization of NFATc4 and activation of NFAT-mediated gene transcription in cultured primary neurons.
Signals transduced by Ca(2+)/calcineurin and NFATc3/c4 pattern the developing vasculature.
Crabtree et al., Stanford, United States. In Cell, 2001
We find that mice with disruptions of both NFATc4 and the related NFATc3 genes die around E11 with generalized defects in vessel assembly as well as excessive and disorganized growth of vessels into the neural tube and somites.
Angiotensin-induced inflammation and novel approaches to treatment.
Luft et al., Berlin, Germany. In Adv Nephrol Necker Hosp, 2000
The subsequent NF-kappa B activation probably involves participation of endothelin signaling and, perhaps, NF-AT3 activation.
The role of NF-AT transcription factors in T cell activation and differentiation.
Avots et al., Würzburg, Germany. In Biochim Biophys Acta, 2000
The family of genuine NF-AT transcription factors consists of four members (NF-AT1 [or NF-ATp], NF-AT2 [or NF-ATc], NF-AT3 and NF-AT4 [or NF-ATx]) which are characterized by a highly conserved DNA binding domain (is designated as Rel similarity domain) and a calcineurin binding domain.
Control of cardiac myosin heavy chain gene expression.
Morkin, Tucson, United States. In Microsc Res Tech, 2000
The beta-MHC gene also is induced together with several other "fetal" genes during cardiac hypertrophy by a mechanism involving Ca(2+)-mediated activation of calcineurin and NF-AT3.
L-type calcium channels and GSK-3 regulate the activity of NF-ATc4 in hippocampal neurons.
Crabtree et al., Stanford, United States. In Nature, 1999
Here we show that NF-ATc4/NF-AT3 in hippocampal neurons can rapidly translocate from cytoplasm to nucleus and activate NF-AT-dependent transcription in response to electrical activity or potassium depolarization.
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