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. 2011 Mar 1;6(3):e16886. doi: 10.1371/journal.pone.0016886

Figure 4. Concentration of dysbindin-1 isoforms A–C in synaptic tissue and relative synaptosomal levels of the isoforms in Western blots (WB) of normal human cerebral cortex and HF.

Figure 4

A: Relative concentrations of the isoforms seen in whole cell lysates (Lys) and cell fractions: cell nuclei (Nuc), synaptosomes (Syn), synaptic vesicles (SV), and postsynaptic densities (PSD) using PA3111. While the samples were from the anterior cingulate cortex (AC), the same distribution pattern was seen in the pSTG and HF, except for lower synaptosomal dysbindin-1A. Bands marked to the left by dots mark likely dysbindin-1 degradation products in SV and PSD fractions. B: Relative concentrations of the dysbindin-1 isoforms in synaptosomes in the pSTG and HF using PA3111 for isoforms 1A and 1C and UPenn 331 for isoform 1B. The higher signal for dysbindin-1B compared to that seen in A probably reflects the much higher affinity of UPenn 331 than PA3111 for this isoform (Figure S1). C: Relative levels of synaptosomal dysbindin-1 isoforms in pSTG and HF compared using normalized PA3111 and UPenn 331 data for all normal cases studied (13 for pSTG, 15 for HF). Dysbindin-1C concentrations in the HF were significantly greater than in the pSTG (p = 0.0002, marked by an asterisk [*]). OD = β-actin normalized optical density of bands in Western blots.