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Fig. 5 | Molecular Medicine

Fig. 5

From: SIGIRR deficiency contributes to CD4 T cell abnormalities by facilitating the IL1/C/EBPβ/TNF-α signaling axis in rheumatoid arthritis

Fig. 5

Enhanced activity of C/EBPβ in Sigirr −/− CD4 T cells upon IL-1β stimulation. A Cell lysates from wild-type and Sigirr −/− CD4 T cells (n = 2) treated with IL-1β (10 ng/ml) for 30 min were analyzed by SDS–PAGE followed by western blotting using antibodies for the indicated molecules. The quantification of each immunoblot is labeled under each band, and the molecular weight (kDa) is displayed on the right side. B Two classical binding motifs of transcription factor C/EBPβ notated by JASPER database. C Schematic representation of C/EBPβ binding sites for TNF-α promotor sequence (upper, homo sapiens and lower, mus musculus) and those binding site-containing nucleotide sequences are shown at right. D UCSC genome track view of C/EBPβ ChIP-seq signals in different loci of TNF-α genes and promotor regions, 2 kb nucleotides relative to the transcriptional start site of TNF-α, are shaded in blue. The upper panel shows the binding signal to Homo sapiens TNF-α genes in monocyte THP-1, leukemia cell MV4;11, epididymis epithelial cells. The lower panel displays the binding signal to Mus musculus TNF-α genes in macrophage MIN, microglial cell BV2 and bone marrow-derived macrophages. Raw ChIP-seq data and treatment protocols are available in the Gene Expression Omnibus (GEO) database (https://www.ncbi.nlm.nih.gov/geo/) under the accession numbers GSM3112102, GSM2345027, GSM1010802, GSM2663837, GSM1315484, and GSM2974847

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