Fig. 3.
Fig. 3. Characterization of constitutive nuclear NF-κB complexes in ARP-1 cells. (A) For competitive EMSA, NEs prepared from untreated parental ARP-1 transfectants were incubated with either a 10- or 50-fold molar excess of unlabeled wild-type or mutated κB oligonucleotides and assayed for their ability to compete with radiolabeled wild-type κB probe in a standard EMSA. Arrows indicate two specific NF-κB complexes. (B) p50:p50 and p50:p65 dimers bind to the κB site. Supershift EMSA was performed using whole cell extracts prepared from parental ARP-1 transfectants. When marked, antibodies specific for p50, p65, c-Rel, and USF and E2F-1 (two control unrelated antibodies) were incubated in an EMSA reaction. The positions of p50:p50 and p50:p65 NF-κB complexes are indicated by arrows.

Characterization of constitutive nuclear NF-κB complexes in ARP-1 cells. (A) For competitive EMSA, NEs prepared from untreated parental ARP-1 transfectants were incubated with either a 10- or 50-fold molar excess of unlabeled wild-type or mutated κB oligonucleotides and assayed for their ability to compete with radiolabeled wild-type κB probe in a standard EMSA. Arrows indicate two specific NF-κB complexes. (B) p50:p50 and p50:p65 dimers bind to the κB site. Supershift EMSA was performed using whole cell extracts prepared from parental ARP-1 transfectants. When marked, antibodies specific for p50, p65, c-Rel, and USF and E2F-1 (two control unrelated antibodies) were incubated in an EMSA reaction. The positions of p50:p50 and p50:p65 NF-κB complexes are indicated by arrows.

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