Target intelligence / Profile preview

Small nucleolar RNA SNORD115-15 (SNORD115-15)

Target
SNORD115-15
Molecular classification
Small nucleolar RNA (snoRNA), C/D box snoRNA, Non-coding RNA
01

Overview

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.

Other names
HBII-52-15SNORD115-15MBII-52-15 (mouse ortholog)
02

Biological functions

Guide RNA for RNA modification (mainly 2'-O-methylation)Regulation of alternative splicing (notably of serotonin receptor 2C mRNA, HTR2C)Modulation of post-transcriptional RNA processing
03

Disease associations

Prader-Willi syndrome (PWS)Neurodevelopmental disorders (linked via imprinting region)Potential involvement in autism spectrum-like features (in mouse models)Other neuropsychiatric diseases (implicated via serotonin receptor regulation)
04

Safety considerations

Genomic redundancy complicates targeting or knock-downHighly structured RNA, challenging for oligonucleotide therapeutics
05

Biomarkers

Absence of expression in PWS patients (brain-specific marker)

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