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. 2016 May 4;11(5):e0154884. doi: 10.1371/journal.pone.0154884

Fig 4. Transcriptional activation of NF-κB in LS8 cells transfected with wild-type and mutant EDA1 proteins.

Fig 4

(A-X) Immunofluorescence of NF-κB subunit p65 (p65, red; DAPI, blue) in LS8 cells transfected with wild-type EDA1 (A-C), pCR3 (D-F), non-syndromic tooth agenesis-causing EDA1 mutants (G-R), and HED-causing EDA1 mutants (S-X). White arrows indicate the nuclear staining of p65. (Y) Quantitation of the ratio of p65- positive nuclei number. (Z) Dual luciferase assay revealed that transcriptional NF-κB activation induced by mutant EDA1 proteins was significantly reduced compared with that of wild-type EDA1. *, P<0.05; **, P<0.01; WT, wild-type.