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Immunity ; 16(6): 881-95, 2002 Jun.
Article in English | MEDLINE | ID: mdl-12121669

ABSTRACT

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.


Subject(s)
Apoptosis , DNA-Binding Proteins/biosynthesis , Nuclear Proteins , T-Lymphocytes, Regulatory/physiology , Transcription Factors/biosynthesis , Alternative Splicing , Animals , Base Sequence , DNA Methylation , DNA-Binding Proteins/genetics , Deoxyribonuclease I/metabolism , Electrophoresis, Polyacrylamide Gel , Homeostasis , Humans , Jurkat Cells , Mice , Mice, Inbred BALB C , Molecular Sequence Data , NFATC Transcription Factors , Poly A/metabolism , Promoter Regions, Genetic , Transcription Factors/genetics , Transcription, Genetic
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