Foxp3 interacts with nuclear factor of activated T cells and NF-kappa B to repress cytokine gene expression and effector functions of T helper cells.
By E. Bettelli, Maryam Dastrange, M. Oukka. Proceedings of the National Academy of Sciences of the United States of America, 2005
606 citations recorded by the source corpus.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/03cd3033cb3d154fb85676fca35ea2966bca5aea
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In Immunology
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Citations in the corpus
- Genetic analysis of host resistance: Toll-like receptor signaling and immunity at large. (2006, background): “Recent studies have shown that the transcription factors NFAT and AP-1 are constitutively activated in CD4+ T cells from sf/Y mice (11).”
- FOXP3+ regulatory T cells in the human immune system (2010, background): “, and lacks amino-terminal residues that may mediate the interaction with nuclear factor of activated T cells (NFAT) and the resulting transcriptional repressio”
- Dual functions for the endoplasmic reticulum calcium sensors STIM1 and STIM2 in T cell activation and tolerance (2008, background): “and a requirement for NFAT in Foxp3-mediated transcription and suppressor functio”
- FOXP3 controls regulatory T cell function through cooperation with NFAT. (2006, positive): “An alternative possibility, based on the finding that NFAT and FOXP3 physically interact in cell lysates (Bettelli et al., 2005), is that FOXP3 represses NFAT-driven cytokine transcription by sequestering NFAT away from DNA.”
- NF-κB activation as a pathological mechanism of septic shock and inflammation (2006, neutral): “Interactions between NF- B and STAT1 (81), E2F transcription factor 1 (43), mammalian transcriptional repressor RBP-J (CBF1) (178), IFN-inducible p202a protein (150), forkhead box P3 (Foxp3) (19), and zincfinger protein ZAS3 (99) are antagonistic and unreciprocal, inhibiting NF- B-mediated transcrip”