ArticleMolecular and cellular biology2016
NFAT2 Isoforms Differentially Regulate Gene Expression, Cell Death, and Transformation through Alternative N-Terminal Domains.
Article in Molecular and cellular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Two Faces of NFAT Transcription Factors in LymphocytesBiomolecules · 2026Review
- A DYRK inhibitor ameliorates glucose homeostasis and increases incretin-producing cells in diabetic mice.Journal of molecular endocrinology · 2026Article
- NFATc1-mediated activation of the pentose phosphate pathway and cell cycle dysregulation collectively drive tumor progression.Oncogenesis · 2025Article
- SF3B1 mutation accelerates the development of CLL via activation of the mTOR pathway.JCI insight · 2025Article
- Determination of Inhibitory Effect of PKM2 Enzyme and Antitumoral Activity of Novel Coumarin-naphthoquinone Hybrids.Current medicinal chemistry · 2025Article
- The alpha-synuclein oligomers activate nuclear factor of activated T-cell (NFAT) modulating synaptic homeostasis and apoptosis.Molecular medicine (Cambridge, Mass.) · 2023Article
- Chemoselective Synthesis of Mannich Adducts from 1,4-Naphthoquinones and Profile as Autophagic Inducers in Oral Squamous Cell Carcinoma.Molecules (Basel, Switzerland) · 2022Article
- Pro-Apoptotic Antitumoral Effect of Novel Acridine-Core Naphthoquinone Compounds against Oral Squamous Cell Carcinoma.Molecules (Basel, Switzerland) · 2022Article
- Isoform-Selective NFAT Inhibitor: Potential Usefulness and Development.International journal of molecular sciences · 2021Review
- NFAT2 overexpression suppresses the malignancy of hepatocellular carcinoma through inducing Egr2 expression.BMC cancer · 2020Article
- Transcription Factors in Cancer: When Alternative Splicing Determines Opposite Cell Fates.Cells · 2020Review
- B cells infected with Type 2 Epstein-Barr virus (EBV) have increased NFATc1/NFATc2 activity and enhanced lytic gene expression in comparison to Type 1 EBV infection.PLoS pathogens · 2020Article
- Axonal Protection by Tacrolimus with Inhibition of NFATc1 in TNF-Induced Optic Nerve Degeneration.Neurochemical research · 2019Article
- NFAT1 and NFAT2 Differentially Regulate CTL Differentiation Upon Acute Viral Infection.Frontiers in immunology · 2019Article
- NFATc1 is a tumor suppressor in hepatocellular carcinoma and induces tumor cell apoptosis by activating the FasL-mediated extrinsic signaling pathway.Cancer medicine · 2018Article
- Priming of transcriptional memory responses via the chromatin accessibility landscape in T cells.Scientific reports · 2017Article
- Cell cycle and apoptosis regulation by NFAT transcription factors: new roles for an old player.Cell death & disease · 2016Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NFAT (nuclear factor of activated T cells) family of transcription factors is composed of four calcium-responsive proteins (NFAT1 to -4). The NFAT2 (also called NFATc1) gene encodes the isoforms NFAT2α and NFAT2β that result mainly from alternative initiation exons that provide two different N-terminal transactivation domains. However, the specific roles of the NFAT2 isoforms in cell physiology remain unclear. Because previous studies have shown oncogenic potential for NFAT2, this study emphasized the role of the NFAT2 isoforms in cell transformation. Here, we show that a constitutively active form of NFAT2α (CA-NFAT2α) and CA-NFAT2β distinctly control death and transformation in NIH 3T3 cells. While CA-NFAT2α strongly induces cell transformation, CA-NFAT2β leads to reduced cell proliferation and intense cell death through the upregulation of tumor necrosis factor alpha (TNF-α). CA-NFAT2β also increases cell death and upregulates Fas ligand (FasL) and TNF-α in CD4(+) T cells. Furthermore, we demonstrate that differential roles of NFAT2 isoforms in NIH 3T3 cells depend on the N-terminal domain, where the NFAT2β-specific N-terminal acidic motif is necessary to induce cell death. Interestingly, the NFAT2α isoform is upregulated in Burkitt lymphomas, suggesting an isoform-specific involvement of NFAT2 in cancer development. Finally, our data suggest that alternative N-terminal domains of NFAT2 could provide differential mechanisms for the control of cellular functions.
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