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Small nucleolar RNA SNORD115-15 is a brain-specific, non-coding RNA belonging to the C/D box family of snoRNAs, defined by characteristic C (UGAUGA) and D (CUGA) box motifs[1][3]. It is one member of a tandem repeat cluster (SNORD115/HBII-52 family, with >40 human copies) located in the imprinted Prader-Willi syndrome region on chromosome 15q11–q13[4][1]. SNORD115-15 acts primarily as a guide RNA; its best-characterized function is a highly conserved 18-nucleotide antisense element complementing the serotonin receptor 2C (HTR2C, 5-HT2CR) pre-mRNA, where it influences exon Vb inclusion and A-to-I RNA editing, thus modulating the functional output of the receptor[2][3][4]. The precise functional mechanism remains debated: some studies suggest direct guidance of site-specific 2’-O-methylation, while others indicate SNORD115 acts by interfering with splicing silencers to promote exon inclusion independently of methylation[2][3]. In humans and mice, loss of SNORD115 is linked to PWS and abnormal neurodevelopment; overexpression in mouse models relates to autism-like behaviors[3][4]. SNORD115 does not encode for any protein, nor is it a classical therapeutic target receptor/enzyme/transporter, but it underpins critical post-transcriptional RNA regulation in the brain[1][2][3]. No direct pharmacological modulators or small-molecule drugs target SNORD115-15 itself, though its pathway implicates the serotonin system—a major pharmacological axis in psychiatry.
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