6533b872fe1ef96bd12d43fd
RESEARCH PRODUCT
Autoregulation of NFATc1/A Expression Facilitates Effector T Cells to Escape from Rapid Apoptosis
Edgar SerflingDimitri TyrsinFriederike Berberich-siebeltEriks JankevicsSergei ChuvpiloElizaveta FeoktistovaMithilesh Kumar JhaEdgar SchmittAndris AvotsBrigitte Santner-nananJan Schulze-luehrmannDenis MorozAnneliese SchimplAskar M. AkimzhanovThomas Königsubject
Gene isoformTranscription GeneticMolecular Sequence DataImmunologyApoptosisBiologyT-Lymphocytes RegulatoryJurkat CellsMiceExonAnimalsDeoxyribonuclease IHomeostasisHumansImmunology and AllergyPromoter Regions GeneticTranscription factorMice Inbred BALB CBase SequenceNFATC Transcription Factorsintegumentary systemEffectorNuclear ProteinsNFATDNA MethylationMolecular biologyChromatinDNA-Binding ProteinsAlternative SplicingInfectious DiseasesCpG siteApoptosisElectrophoresis Polyacrylamide GelPoly ATranscription Factorsdescription
AbstractThreshold 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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2002-06-01 | Immunity |