Genomic binding of ARID3A and STAT1. (A) Quantitative RT-PCR of Arid3a and IFN-related genes in Arid3a^+/+, ^+/−, and ^−/− E11.5 AGM; n = 3-8. Error bars indicate SEM. (B) Immunostaining of E11.5 Arid3a WT and KO AGMs for phospho-Stat1. Scale bar = 100 μm. (C) ChIP-seq tracks ARID3A and STAT1 at the genomic loci of IFN-αR1 in K562 cells. (D) ChIP-seq tracks ARID3A and STAT1 at the genomic loci of IRF1 in K562 cells. (E) ChIP-seq tracks ARID3A and STAT1 at the genomic loci of STAT1 in K562 cells. (F) ChIP-seq data showing global overlap of binding sites between ARID3A and STAT1 but not the hormone receptor TR4. (G) Immunoprecipitation of ARID3A (left). PI IgG was used as a control. Co-immunoprecipitation of STAT1 with ARID3A (right). K562 cells were exposed for 90 to 120 minutes of IFN-α (0.5 ng/mL). (H) Confirmation of ChIP-seq via quantitative ChIP-PCR in K562 cells normalized by input control; n = 4. Error bars indicate SEM. (I) Confirmation of ChIP-seq via quantitative ChIP-PCR in CB CD34⁺ cells normalized by input control; n = 2. Statistical significance: *P < .05; **P < .01. ao, dorsal aorta; CB, cord blood; cv, cardinal vein; DAPI, 4′,6-diamidino-2-phenylindole; het, heterozygous; IB, immunoblot; IgG, immunoglobulin G; nc, notochord; ns, not signicant; PI, pre-immune; ur, urogenital ridge.