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. 2018 Aug 28;9(67):32841–32854. doi: 10.18632/oncotarget.26003

Figure 5. Pax5A and Pax5B show different activities during late B cell stages.

Figure 5

(A) Expression by QPCR of total Pax5 or specific Pax5 isoforms in resting murine B cells, activated B cells and plasmablasts. Results are expressed as log scale with mean ± SEM of independent experiments. (B) Relative quantification of Cd19 transactivation in Ba/F3 after infection with either eGFP-expressing retrovirus (MIE) or MIE containing PAX5A or PAX5B (C) PAX5A or PAX5B trans-activity was determined using a Luciferase reporter (pCD19-Luc) assay in 293T cells (left panel) or S194 cells (right panel). Results are expressed as mean ± SEM of independent experiments. (D) ChIP was performed on Cd19 promoter (pCD19) and Upf1 intron 9 (as a PAX5 non-target) and using an irrelevant IgG or an anti-PAX5 antibody. Results are expressed as mean of fold change compared to IgG condition ± SEM of independent experiments. (E) ChIP was performed on the hypersensitive sites (hs)1,2 and hs4 elements of the 3′RR in resting splenic B cells or activated B cells (left and right panel respectively) using an irrelevant IgG or a anti-PAX5 antibody. Results are expressed as mean ± SEM of independent experiments. (F) A Luciferase expression B cell specific vector (pVH-luc) containing the IGH 3′RR minilocus (+3′RR) or not (–3′RR) was used in a reporter assay to determine the regulatory function of PAX5A and PAX5B in S194 cells. Results are expressed as mean of fold change compared to IgG condition ± SEM of independent experiments. Ctl: negative control, *p < 0.05; **p < 0.01; ***p < 0,001 (unpaired two-tailed t test).