Autoregulation of NFATc1/A expression facilitates effector T cells to escape from rapid apoptosis - PubMed (original) (raw)
doi: 10.1016/s1074-7613(02)00329-1.
Eriks Jankevics, Dimitri Tyrsin, Askar Akimzhanov, Denis Moroz, Mithilesh Kumar Jha, Jan Schulze-Luehrmann, Brigitte Santner-Nanan, Elizaveta Feoktistova, Thomas König, Andris Avots, Edgar Schmitt, Friederike Berberich-Siebelt, Anneliese Schimpl, Edgar Serfling
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- PMID: 12121669
- DOI: 10.1016/s1074-7613(02)00329-1
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Autoregulation of NFATc1/A expression facilitates effector T cells to escape from rapid apoptosis
Sergei Chuvpilo et al. Immunity. 2002 Jun.
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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.
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