Autoregulation of NFATc1/A Expression Facilitates Effector T Cells to Escape from Rapid Apoptosis
Copyright policy )Autoregulation of NFATc1/A Expression Facilitates Effector T Cells to Escape from Rapid Apoptosis
Threshold levels of individual NFAT factors appear to be critical for apoptosis induction in effector T cells. In these cells, the short isoform A of NFATc1 is induced to high levels due to the autoregulation of the NFATc1 promoter P1 by NFATs. P1 is located within a CpG island in front of exon 1, represents a DNase I hypersensitive chromatin site, and harbors several sites for binding of inducible transcription factors, including a tandemly arranged NFAT site. A second promoter, P2, before exon 2, is not controlled by NFATs and directs synthesis of the longer NFATc1/B+C isoforms. Contrary to other NFATs, NFATc1/A is unable to promote apoptosis, suggesting that NFATc1/A enhances effector functions without promoting apoptosis of effector T cells.
- Johannes Gutenberg University of Mainz Germany
- Pathologisches Institut Germany
- University of Würzburg Germany
- University of Latvia Latvia
- University Hospital Würzburg Germany
Immunology, Molecular Sequence Data, Apoptosis, T-Lymphocytes, Regulatory, Jurkat Cells, Mice, Immunology and Allergy, Animals, Deoxyribonuclease I, Homeostasis, Humans, Promoter Regions, Genetic, Mice, Inbred BALB C, Base Sequence, NFATC Transcription Factors, Nuclear Proteins, DNA Methylation, DNA-Binding Proteins, Alternative Splicing, Infectious Diseases, Electrophoresis, Polyacrylamide Gel, Poly A, Transcription Factors
Immunology, Molecular Sequence Data, Apoptosis, T-Lymphocytes, Regulatory, Jurkat Cells, Mice, Immunology and Allergy, Animals, Deoxyribonuclease I, Homeostasis, Humans, Promoter Regions, Genetic, Mice, Inbred BALB C, Base Sequence, NFATC Transcription Factors, Nuclear Proteins, DNA Methylation, DNA-Binding Proteins, Alternative Splicing, Infectious Diseases, Electrophoresis, Polyacrylamide Gel, Poly A, Transcription Factors
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