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. Author manuscript; available in PMC: 2016 Sep 3.
Published in final edited form as: Cell Stem Cell. 2015 Aug 13;17(3):316–328. doi: 10.1016/j.stem.2015.07.017

Figure 7. Heterozygous NRXN1 inactivation stabilizes CASK protein levels in human neurons.

Figure 7

(A) Quantifications of selected total mRNA levels in matched control vs. NRXN1-mutant iN cells as measured by quantitative RT-PCR. Average ΔCt values (normalized to synapsin-1 mRNA) were converted to a ratio of control/mutant and plotted on a logarithmic scale.

(B & C) Quantifications of protein levels in control iN cells and in iN cells with heterozygous NRXN1 mutations (Syt1, synaptotagmin-1; Cpx 1/2, complexin-1 and -2; Syb2, synaptobrevin-2). Protein levels were determined by quantitative immunoblotting using fluorescently labeled secondary antibodies (B, representative immunoblots; C, summary graphs). NeuN was used as a loading control.

(D) Quantifications of CASK protein levels in control and NRXN1-mutant human neurons using a different antibody to CASK that was used from panels B & C. iN cells from both clones with heterozygous cTr NRXN1 mutations and neurons obtained by a standard protocol (Fig. 5) were analyzed.

All quantitative data are normalized for the controls analyzed in parallel, and expressed as means ± SEM (n=3–5 independent cultures). Statistical analyses were performed by Student’s t-test comparing test samples to control (*p<0.05).