Cited by 357Signaling Pathways in DiseaseProtein Kinase Regulation and GTPase SignalingGenomics and Chromatin Dynamics

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Nuclear Accumulation of NFAT4 Opposed by the JNK Signal Transduction Pathway

Chow, Chi-Wing, Rincón, Mercedes, Cavanagh, Julie, Dickens, Martin, Davis, Roger J.·1997·Science

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Abstract

The nuclear factor of activated T cells (NFAT) group of transcription factors is retained in the cytoplasm of quiescent cells. NFAT activation is mediated in part by induced nuclear import. This process requires calcium-dependent dephosphorylation of NFAT caused by the phosphatase calcineurin. The c-Jun amino-terminal kinase (JNK) phosphorylates NFAT4 on two sites. Mutational removal of the JNK phosphorylation sites caused constitutive nuclear localization of NFAT4. In contrast, JNK activation in calcineurin-stimulated cells caused nuclear exclusion of NFAT4. These findings show that the nuclear accumulation of NFAT4 promoted by calcineurin is opposed by the JNK signal transduction pathway.

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Authors: Chow, C.-W., Rincón, M., Cavanagh, J., Dickens, M., & Davis, R. J.
Affiliations: University of Vermont (US)
C.-W. Chow, J. Cavanagh, M. Dickens, R. J. Davis, Howard Hughes Medical Institute, Program in Molecular Medicine, Department of Biochemistry and Molecular Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Corresponding author: Davis, Roger J.
ORCID: Cavanagh, Julie
Dickens, Martin
Davis, Roger J.
Venue: Science
Publisher: American Association for the Advancement of Science (AAAS)
Published: 1997-11-28
Volume: 278
Issue: 5343
Pages: 1638-1641
ISSN: 0036-8075 (ISSN-L)
1095-9203
DOI: 10.1126/science.278.5343.1638
OpenAlex: W2053010478
Cited by: 357
References: 24
Citations by year: 2026: 1 · 2025: 3 · 2024: 2 · 2023: 2 · 2022: 4 · 2021: 2 · 2020: 11 · 2019: 3 · 2018: 3 · 2017: 4 · 2016: 6 · 2015: 7 · 2014: 8 · 2013: 3 · 2012: 15
FWCI: 7.70
Type: journal article
Language: en
Open access: closed
Locations: Science (publishedVersion)
PubMed (publishedVersion)
The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
Funders: National Institutes of Health (5r01ca058396-09)
National Cancer Institute (CA 58396, CA65831)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Keywords: NFAT4, NFAT, c-Jun N-terminal kinase, calcineurin, JNK phosphorylation, nuclear import, nuclear accumulation, transcription factor regulation, signal transduction
MeSH terms: Animals, Binding Sites, Cell Line, Cell Nucleus, Cytoplasm, DNA-Binding Proteins, Humans, Mutation, Nuclear Proteins, Phosphorylation, Protein Kinases, Recombinant Fusion Proteins, T-Lymphocytes, Transcription Factors, Transcription, Genetic, Signal Transduction, Cyclosporine, Calcium-Calmodulin-Dependent Protein Kinases, Jurkat Cells, COS Cells, Calcineurin, Mitogen-Activated Protein Kinases, Mitogen-Activated Protein Kinase Kinases, JNK Mitogen-Activated Protein Kinases, NFATC Transcription Factors, Calcineurin Inhibitors

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Nuclear Accumulation of NFAT4 Opposed by the JNK Signal Transduction Pathway

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