Figure 2
Epigenetic changes in GPPP gene promoters in response to NaBu treatment. (A) Histone 3 and histone 4 acetylation (H3Ac; H4Ac) levels assessed by ChIP-RQ-PCR in WT B cells at baseline and after NaBu treatment. A GAPDH promoter amplicon is used as a positive control. GW10, an amplicon in a region devoid of genes on chromosome 10 is shown as a negative control (n = 3). (B-C) HAT and HDAC binding, respectively, at the GPPP gene promoters in WT B cells in the presence of NaBu. CBP, GCN5, and p300 binding assessed by ChIP-RQ-PCR after 5-hour treatment with NaBu (n = 3). (D) Pol II binding on the GPPP gene promoters and 2 gene body areas of G6PD (GB1 and GB2) in WT B cells after 0 to 24 hours of treatment with NaBu (n = 3). Enrichment of binding in the target areas using specific antibody and immunoglobulin G (IgG) controls is calculated as percentage of input throughout (n = 3). *P < .05; **P < .01; ***P < .001

Epigenetic changes in GPPP gene promoters in response to NaBu treatment. (A) Histone 3 and histone 4 acetylation (H3Ac; H4Ac) levels assessed by ChIP-RQ-PCR in WT B cells at baseline and after NaBu treatment. A GAPDH promoter amplicon is used as a positive control. GW10, an amplicon in a region devoid of genes on chromosome 10 is shown as a negative control (n = 3). (B-C) HAT and HDAC binding, respectively, at the GPPP gene promoters in WT B cells in the presence of NaBu. CBP, GCN5, and p300 binding assessed by ChIP-RQ-PCR after 5-hour treatment with NaBu (n = 3). (D) Pol II binding on the GPPP gene promoters and 2 gene body areas of G6PD (GB1 and GB2) in WT B cells after 0 to 24 hours of treatment with NaBu (n = 3). Enrichment of binding in the target areas using specific antibody and immunoglobulin G (IgG) controls is calculated as percentage of input throughout (n = 3). *P < .05; **P < .01; ***P < .001

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