Figure 4.

Evidence for the regulation of the GABAR β1 promoter by NRF-1. (A) Primary cortical neurons were co-transfected with 2 μg of wild type GABRB1p (wtGABRB1p) or the NRF-1 binding site mutant (mGABRB1p) and 1 μg of empty vector pcDNA3 or the NRF-1:VP16 fusion construct. Cells were assayed for luciferase activity 24 h after transfection. Data represent the average ± SEM (n = 5 independent transfections) of luciferase activity relative to wild type GABRB1p in the absence of NRF-1:VP16. **p < 0.01, ****p < 0.0001, and “ns” (non-specific) represent presence or absence respectively of significance according to one-way ANOVA with Tukey’s multiple comparisons test. (B) Primary cortical neurons were co-transfected with either pcDNA3 or the dominant negative variant of NRF-1 (NRF-1 DN) and GABRB1p reporter (2 μg). Twenty-four hours after transfection, cells were assayed for luciferase activity. Data represent the average ± SEM of n = 6 independent transfections (see above), normalized to wtGABRB1p and pcDNA3. *p < 0.05, Student’s t-test. This dataset was originally published in the thesis of Li (2015).