Fig. 9

Stat1 may recruit Rab11fip1 to regulate SC differentiation. A Stat1-binding regions obtained by ChIP-seq. The colored rectangle annotation represent peaks at the promoter (defined as ≤ 1000 bp), the promoter (defined as 1000 − 3000 bp), downstream of thepromoter (defined as ≤ 300 bp), 5’ UTR, 3’UTR, exon, intron or distal intergenic. B Distribution of enrichment intensity of ChIP-seq reads in the proximity of the transcription start site (TSS) (up), and consensus motifs at Stat1 bound sequences (down). C GO enrichment analysis of peak-related genes (bubble diagram). D Venn diagram shows overlap of genes with top 500 peak in the promoter related genes and 386 differentially expressed genes (p < 0.05 and Fold change ≥ 2) between Stat1 knockdown groups and the control groups. E Histograms visualizing Stat1 binding around the 4 overlapping genes (Ano1, Nts, C1qb and Rab11fip1) locus. “Peak number” represents the plausibility ranking of the peak. F ChIP-qPCR for Stat1 occupancy on the Ano1, Nts, C1qb and Rab11fip1 promoters in differentiating SCs. T-test, **p < 0.01, ***p < 0.01, n = 3 per group. G Luciferase activity of Ano1, Nts, C1qb and Rab11fip1 promoter and mutant promoter in HEK293 cells co-transfected with pGV141-Stat1 (Stat1 overexpression plasmid) plus an plasmid containing the Renilla luciferase gene. T-test, ***p < 0.01, n = 3 per group. H Western blots showing the expression level of Rab11fip1 and MAG in differentiated SCs treated with Rab11fip1-siRNA and Scramble. The histograms showing that knockdown Rab11fip1 reduces MAG expression in differentiated SCs. T-test, ***p < 0.001 vs Scramble, n = 3 per group