Figure 6
Figure 6. LMP2A is the key factor of EBV inhibiting the expression of E47 and PU.1 and their downstream genes. (A) Expression of EBNA1, LMP1, LMP2A, E47, PU.1, and β-actin in various pairs of uninfected primary B cells and EBV-immortalized LCLs was detected by western blotting. β-actin served as an internal control. (B-H) The LCL lines B36, B37, B44, and B47 were infected with shLuc or shLMP2A lentiviruses. After 5 days, the RNA and protein were harvested. Expression levels of the LMP2A (B), E47 (C), PU.1 (D), CIITA (E), HLA-DRA (F), HLA-DRB (G), and CD74 (H) transcripts were measured by RT-Q-PCR. (I) LCL B47 cells were infected with PU.1 or FD-E47 expression lentiviruses. Expression of E47, PU.1, CD74, MHC class II, and LMP2A was analyzed by western blotting. β-actin was detected as an internal control. (Paired t test, *P < .05; **P < .01). Each experiment was performed 3 times, and 1 representative is shown.

LMP2A is the key factor of EBV inhibiting the expression of E47 and PU.1 and their downstream genes. (A) Expression of EBNA1, LMP1, LMP2A, E47, PU.1, and β-actin in various pairs of uninfected primary B cells and EBV-immortalized LCLs was detected by western blotting. β-actin served as an internal control. (B-H) The LCL lines B36, B37, B44, and B47 were infected with shLuc or shLMP2A lentiviruses. After 5 days, the RNA and protein were harvested. Expression levels of the LMP2A (B), E47 (C), PU.1 (D), CIITA (E), HLA-DRA (F), HLA-DRB (G), and CD74 (H) transcripts were measured by RT-Q-PCR. (I) LCL B47 cells were infected with PU.1 or FD-E47 expression lentiviruses. Expression of E47, PU.1, CD74, MHC class II, and LMP2A was analyzed by western blotting. β-actin was detected as an internal control. (Paired t test, *P < .05; **P < .01). Each experiment was performed 3 times, and 1 representative is shown.

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