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.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Alternative Splicing
-
Animals
-
Apoptosis*
-
Base Sequence
-
DNA Methylation
-
DNA-Binding Proteins / biosynthesis*
-
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
-
Nuclear Proteins*
-
Poly A / metabolism
-
Promoter Regions, Genetic
-
T-Lymphocytes, Regulatory / physiology*
-
Transcription Factors / biosynthesis*
-
Transcription Factors / genetics
-
Transcription, Genetic
Substances
-
DNA-Binding Proteins
-
NFATC Transcription Factors
-
NFATC1 protein, human
-
Nfatc1 protein, mouse
-
Nuclear Proteins
-
Transcription Factors
-
Poly A
-
Deoxyribonuclease I