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Figure 5 | Molecular Autism

Figure 5

From: Transcriptional and functional complexity of Shank3 provides a molecular framework to understand the phenotypic heterogeneity of SHANK3 causing autism and Shank3 mutant mice

Figure 5

Differential isoform-specific expression and alternative splicing of Shank3 induced by a histone deacetylase (HDAC) inhibitor. (A) q-PCR analysis of Shank3 isoforms in cultured mouse cortical neurons after treatment with 5 μM trichostatin A (TSA), a potent HDAC inhibitor, for 18 hours. (B) Western blot showed reduced Shank3 proteins after TSA treatment. (C) Quantification for Shank3 proteins in (B) . (D) Differential changes of alternative splicing of Shank3 after TSA treatment. (E) Alternative splicing for Shank3 E10–12S III to IV was increased. (F) Splicing for E18S II of Shank3e was not changed. (G) Splicing for E18S IV of Shank3e-1 was decreased. All data are shown as mean ± SEM. * P <0.05, # P <0.002, compared to the control group, two tail t-test, n = 4 each group.

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