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- W4313383669 abstract "Abstract Unresolved inflammation is an underlying reason for several immune and inflammatory diseases as well as cancer. Both initiation and resolution of inflammatory response rely largely on the genes induced by NF-kB/Rel family of transcription factors. Previous studies have categorized NF-kB family proteins as transcriptional activators (homo or hetero dimers containing RelA, RelB or c-Rel) and transcriptional inhibitors (homodimers of p50 or p52). Here, we report the function of the subunit c-Rel with a transactivation domain, as a transcriptional repressor of selected proinflammatory genes. Genetic deletion of c-Rel enhances the expression of a subset of proinflammatory genes and also potentiates the expression of TNF-induced RelA-dependent mediators of inflammation. Interestingly, v-Rel, the viral homologue of c-Rel, also possesses this repressive function, indicating that the repressive function of c-Rel is evolutionarily conserved. We also found that c-Rel’s ability to repress transcription depends on it competency to bind consensus NF-kB-binding sites in the DNA. Our findings reveal a novel role of c-Rel as a transcriptional repressor in the maintenance of inflammatory homeostasis." @default.
- W4313383669 created "2023-01-06" @default.
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- W4313383669 date "2018-05-01" @default.
- W4313383669 modified "2023-10-01" @default.
- W4313383669 title "NF-kB c-Rel Dictates the Inflammatory Threshold by Acting as a Transcriptional Repressor" @default.
- W4313383669 doi "https://doi.org/10.4049/jimmunol.200.supp.109.9" @default.
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