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Table 1.

SNPs that modify miRNA binding sites according to PolymiRTS Database.

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Table 2.

Analysis output with miRecords, that integrates predicted miRNA targets produced by 11 miRNA target prediction programs.

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Table 2 Expand

Figure 1.

Multiple genome alignment of BDNF 3′UTR in the region of polymorphic sites rs11030100 and rs11030099 (in bold letters).

Sequence analysis shows that sites are highly conserved among primate genomes.

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Figure 1 Expand

Table 3.

Allele and genotype frequencies of BDNF polymorphisms rs11030100-rs11030099 in control subjects and schizophrenic patients.

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Table 3 Expand

Figure 2.

Luciferase assays for validation of miR-26a and -26b binding to BDNF 3′UTR.

HeLa cells were independently transfected with control plasmid (pRL-TK) or each of the two reporter plasmid (pluc-BDNF C–G, anc, and pluc-BDNF A–T, der) with either miR-26a or miR-26b. Data are presented as the normalized activity of different reporter genes. Introduction of exogenous miR-26a and miR-26b represses reporter activity of pluc-BDNF C–G but has no effect on pluc-BDNF A–T. Data represent the mean of five independent experiments +SD (p<0.05).

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Figure 3.

Schematic representation of base pairing between miR-26a sequence and BDNF 3′UTR ancestral (C–G) and derivative (A–T) alleles of rs11030100 and rs11030099 polymorphic sites.

MiR-26b has the same seed binding sequence.

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Figure 3 Expand

Table 4.

Allele and genotype frequencies of BDNF polymorphism rs6265 (Val66Met) in control subjects and schizophrenic patients.

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Table 4 Expand