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Figure 2 | Molecular Autism

Figure 2

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 2

Differential expression of Shank3 isoforms across brain regions and development. (A–E) q-PCR of Shank3 major isoforms in different brain regions. (G–K) q-PCR of Shank3 isoforms in brain across development. The crossing point (CP) values of each isoform were normalized to that of a housekeeping gene, Rpl13a. For brain regions: OB, olfactory bulb; CX, cortex; ST, striatum; HP, hippocampus; TH, thalamus; AD, amygdala; CB, cerebellum. For different ages: P1, postnatal day 1; P5, postnatal day 5; P10, postnatal day 10; P15, postnatal day 15; 4 W, 4 weeks; 3 M, 3 months; 12 M, 12 months. (F and L) Western blot analysis using an antibody produced from an epitope at the C-terminus of SHANK3 protein (amino acids 1431 to 1590) for different mouse brain regions (F) or at different ages (L) . The predicted bands for Shank3a (185KD), Shank3c/d (128KD/127KD), and Shank3e (118KD) are indicated by arrows. All of these bands migrate a little higher than prediction, which may be caused by post-translational modifications of Shank3 proteins. Shank3b was not detectable as the epitope of the antibody was spliced out in this isoform. All data are shown as mean ± SEM.

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Molecular Autism

ISSN: 2040-2392