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. 2010 Apr 12;38(15):4970–4984. doi: 10.1093/nar/gkq245

Figure 2.

Figure 2.

The level of synergy is highly dependent on the sumoylation status of c-Myb. CV-1 cells were transfected with reporters containing one or four MREs [1×MRE(GG)-MYC or 4×MRE(GG)-MYC] and plasmids encoding (A) c-Myb wild-type, c-Myb 2KR or a 2KR-mutant fused to SUMO-1, (B) c-Myb wild-type, c-Myb with individual SUMO-conjugation sites mutated from glutamate to alanine (E505A, E529A) or with both sites mutated (2EA), (C) c-Myb wild-type or the oncogenic version AMV v-Myb, or (D) c-Myb wild-type or a SUMO-negative c-Myb 2KR, with or without the SUMO-protease SENP1 or SENP1 mutant as indicated. The results are presented as SF ± SEM. Western controls shown in (A) were analyzed using anti-c-Myb (5E11) and anti-GAPDH antibodies. (E) CV-1 cells were co-transfected with a plasmid encoding c-Myb wild-type (1.0 µg) and either SENP1 or SENP1 mutant (0.25 or 0.50 µg) to visualize changes in the sumoylation pattern. The cells were lysed directly in SDS–PAGE loading buffer to maintain the modifications. c-Myb-S and c-Myb-2S: c-Myb modified with one or two SUMO proteins, respectively.