Fig. 4.
Fig. 4. Raji cells were treated with 0.3 μmol/L 5-aza-2′-deoxycytidine for 9 days to demethylate the DAP-Kinase CpG island, placed in normal media for 7 days, and then treated with 1,000 U/mL γ interferon for 11 days. (A) MSP of DAP-Kinase in Raji cells. The methylation status of the DAP-Kinase CpG island was checked on days 0, 2, 5, and 9 of 5-aza-2′-deoxycytidine treatment (D0-9-A) and then after the combined 7 days of normal media and either 11 days of γ interferon (D11-γ) or carrier control (D11-C) media. (B) Raji cell apoptosis. By days 5 and 7, Raji cells exposed to γ interferon underwent significantly more apoptosis than those exposed with carrier control alone (P= .0005 and P = .001, respectively). By days 9 and 11, Raji cells were losing their unmethylated copies of DAP-Kinase and also their sensitivity to γ interferon treatment.

Raji cells were treated with 0.3 μmol/L 5-aza-2′-deoxycytidine for 9 days to demethylate the DAP-Kinase CpG island, placed in normal media for 7 days, and then treated with 1,000 U/mL γ interferon for 11 days. (A) MSP of DAP-Kinase in Raji cells. The methylation status of the DAP-Kinase CpG island was checked on days 0, 2, 5, and 9 of 5-aza-2′-deoxycytidine treatment (D0-9-A) and then after the combined 7 days of normal media and either 11 days of γ interferon (D11-γ) or carrier control (D11-C) media. (B) Raji cell apoptosis. By days 5 and 7, Raji cells exposed to γ interferon underwent significantly more apoptosis than those exposed with carrier control alone (P= .0005 and P = .001, respectively). By days 9 and 11, Raji cells were losing their unmethylated copies of DAP-Kinase and also their sensitivity to γ interferon treatment.

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