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

Immunity. 2002 Jun;16(6):881-95. doi: 10.1016/s1074-7613(02)00329-1.


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


  • DNA-Binding Proteins
  • NFATC Transcription Factors
  • NFATC1 protein, human
  • Nfatc1 protein, mouse
  • Nuclear Proteins
  • Transcription Factors
  • Poly A
  • Deoxyribonuclease I