Supplementary Figure 6: [3H]Ketanserin binding displacement curves, and fluorescence anisotropy assay
From: Antipsychotic-induced Hdac2 transcription via NF-κB leads to synaptic and cognitive side effects
(a) [3H]Ketanserin binding competition curves by atypical antipsychotic (clozapine, paliperidone [active metabolite of risperidone], quetiapine, norquetiapine [active metabolite of quetiapine] and sulpiride), atypical antipsychotic-like (volinanserin) and typical antipsychotic (haloperidol) drugs in HEK293 cells stably expressing human 5-HT2A receptors (n = 2 experiments performed in triplicate). Binding affinities (log Ki values ± s.e.m.) are shown. (b) Schematic representation of the DNA sequences coding for Rel homology regions (RHR) of p65 (residues 19-291) and of p50 (residues 39-350) that were subcloned into the pET-DUET1 expression vector. (c) Fluorescence anisotropy assay shows physical interaction between NF-κB (p65/p50) and the PRDII element from the interferon-β promoter. Fluorescein-labelled DNA fragment of the PRDII element was titrated with different concentrations of NF-κB (p65/p50). DNA fraction bound was plotted as a function of NF-κB (p65/p50) concentration (n = 2 experiments performed in triplicate). Mean ± s.e.m.
