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. 2021 Jan 8;10(1):5. doi: 10.1038/s41389-020-00298-4

Fig. 6. MNT and REL regulate NFKBIA.

Fig. 6

a Schematic representation of human NFKBIA (IκBα) gene showing the peaks for MNT, MYC, MAX (K562 cell line), and SIN3A (GM78), as published by the ENCODE project consortium (genome-euro.ucsc.edu/). b Schematic representation of human NFKBIA (IκBα) gene showing the peaks for MNT binding in the K562 cell line, together with the amplicons analyzed below by ChIP-PCR. The conserved REL-binding sites obtained in the ENCODE project using the TFBS Conserved (tfbsConsSites) track are marked in red rectangles. The E-boxes found in NFKBIA are marked in blue (CACGCG at +907 bp and CACGTG at +1899 bp). c ChIP of MNT (upper panel) or REL (lower panel) in LoVo cells on NFKBIA promoter. TXNIP and MNT −842 used as positive controls and a region upstream MNT promoter (MNT −4729), as a negative control for MNT ChIP. The data are shown as the mean ± S.D., n = 3, **P < 0.05; ***P < 0.01. d Re-ChIP of MNT with REL (MNT → REL) and REL with p50 (REL → p50) in LoVo cells. MNT and REL ChIPs were also re-immunoprecipitated with IgG as a negative control of the technique. The data are shown as the mean ± S.D., n ≥ 3, *P < 0.1. e Model of the MNT regulation of NF-κB signaling. Our results indicate that in a high MNT-levels condition, MNT would be possibly regulating NF-κB signaling by retaining REL dimers in the cytoplasm and by forming a complex with REL in the nucleus that would repress the genes that are normally activated by REL dimers. When we silence MNT, REL dimers are released and they translocate into the nucleus, with the consequent increase in NF-κB target genes and the activation of the pathway.