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. Author manuscript; available in PMC: 2017 Jun 1.
Published in final edited form as: J Cell Physiol. 2015 Nov 4;231(6):1237–1248. doi: 10.1002/jcp.25219

Figure 5. The EphB2 promoter contains three CpG islands and multiple NF-κB binding sites.

Figure 5

The schematic representation of the EphB2 promoter shows three CpG islands −3002 to - 2697, −1428 to −1146, and −803 to −572 base pairs upstream from the transcription start site and three NF-κB binding sites upstream of the transcription start site. The sites containing core sequence nucleotides to the NF-κB are those −730 to −719, −560 to −548, and −232 to −222 base pairs upstream from the transcription start site. The core nucleotides are highlighted in bold. TNF-α increases EPHB2 promoter activity via NF-κB. Human primary neurons were transfected with pGL3-Basic EPHB2 (−840/+83) and showed an increase in EPHB2 promoter activity upon TNF-α treatment via luciferase assay. A further increase was demonstrated with overexpression of NF-κB p65 in combination with TNF-α treatment. This activity was depleted with overexpression of a constitutively active IκBα mutant, which prevents translocation of p65 to the nucleus. Luciferase activity (RLU/s) was normalized to protein concentration in each condition and fold change is represented as RLU/s/µg of protein.