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Immunity. 2002 Jun;16(6):881-95.

Autoregulation of NFATc1/A expression facilitates effector T cells to escape from rapid apoptosis.

Author information

1
Department of Molecular Pathology, Institute of Pathology, University of Wuerzburg, D97080 Wuerzburg, Germany.

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.

PMID:
12121669
DOI:
10.1016/s1074-7613(02)00329-1
[Indexed for MEDLINE]
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