Publikationsdatum:
1997-12-31
Beschreibung:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chow, C W -- Rincon, M -- Cavanagh, J -- Dickens, M -- Davis, R J -- CA58396/CA/NCI NIH HHS/ -- CA65831/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1638-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Program in Molecular Medicine, Department of Biochemistry and Molecular Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9374467" target="_blank"〉PubMed〈/a〉
Schlagwort(e):
Animals
;
Binding Sites
;
COS Cells
;
Calcineurin/metabolism
;
Calcineurin Inhibitors
;
Calcium-Calmodulin-Dependent Protein Kinases/*metabolism
;
Cell Line
;
Cell Nucleus/*metabolism
;
Cyclosporine/pharmacology
;
Cytoplasm/metabolism
;
DNA-Binding Proteins/genetics/*metabolism
;
Humans
;
JNK Mitogen-Activated Protein Kinases
;
Jurkat Cells
;
Mitogen-Activated Protein Kinase Kinases
;
*Mitogen-Activated Protein Kinases
;
Mutation
;
NFATC Transcription Factors
;
*Nuclear Proteins
;
Phosphorylation
;
Protein Kinases/metabolism
;
Recombinant Fusion Proteins/metabolism
;
*Signal Transduction
;
T-Lymphocytes/metabolism
;
Transcription Factors/genetics/*metabolism
;
Transcription, Genetic
Print ISSN:
0036-8075
Digitale ISSN:
1095-9203
Thema:
Biologie
,
Chemie und Pharmazie
,
Informatik
,
Medizin
,
Allgemeine Naturwissenschaft
,
Physik
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