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. 2011 Jun 22;31(25):9159–9169. doi: 10.1523/JNEUROSCI.0302-11.2011

Figure 2.

Figure 2.

Effects of EGF on NF-κB reporter activity, and effects of dominant-negative NF-κB variants on EGF-dependent induction of GLT-1. Cortical astrocyte cultures were infected with lentiviral particles carrying NF-κB luciferase reporter and either dsRED or dominant-negative constructs of IκBα (ΔN or SR). Five days postinfection, cultures were treated with EGF (30 ng/ml) or vehicle for 7 d. A, NF-κB luciferase reporter activity. Luciferase activity was normalized to protein and expressed as a percentage of that measured in control astrocytes without neurons. B, GLT-1 protein levels were analyzed in the same samples. Fifteen micrograms of cell lysate was loaded in each lane. Bottom: Summary of quantification of GLT-1 protein levels normalized to actin and expressed relative to the levels observed in control astrocytes treated with EGF. Data are the mean ± SEM of four independent experiments. ***p < 0.001 compared with corresponding astrocyte control; ###p < 0.001 compared with astrocytes infected with vector control and treated with EGF.