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Small nucleolar RNA SNORD115 (SNORD115)

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

Overview

Small nucleolar RNA SNORD115 is a brain-specific, C/D box non-coding RNA found in mammals, most notable for its role in regulating the alternative splicing and possibly A-to-I editing of serotonin receptor 2C (HTR2C) pre-mRNA[1][2][3][4][5]. It is considered an orphan snoRNA because it does not target rRNAs or snRNAs for 2'-O-methylation, unlike canonical snoRNAs. SNORD115 binds directly to the HTR2C pre-mRNA and promotes production of signaling-competent receptor isoforms, with potential relevance to brain function and neuropsychiatric disease, such as Prader-Willi syndrome. Although highly studied for its potential regulatory roles, SNORD115 is not currently regarded as a therapeutic target, nor are there drugs or established biomarkers associated with its modulation. Key scientific insights: - Not a direct therapeutic target: SNORD115 is not a receptor, enzyme, transporter, or protein drug target; instead, it acts via RNA-based regulation of gene expression[1][2][3][4][5]. - Orphan snoRNA: Unlike most C/D box snoRNAs, it does not guide rRNA methylation but rather modulates alternative splicing and possibly RNA editing events[1][2][4][5]. - Role in disease: Its gene is deleted in most Prader-Willi syndrome patients, possibly contributing to abnormal eating and behavior via effects on serotonin signaling pathways, but knockout studies suggest a modest or context-dependent impact[4]. - Aliases and context: Known commonly as HBII-52 (human), with homologous names in other mammals, and often described in the context of neurogenetic syndromes and pre-mRNA processing[3][4]. - Research use: Investigated in neurobiology, RNA regulation, and epigenetic landscapes, but not under clinical or pharmacological development as a target[1][4][5].

Other names
snoHBII-52HBII-52LOC124902571RBII-52 (rat)MBII-52 (mouse)
02

Biological functions

Alternative splicing regulation (especially HTR2C pre-mRNA)RNA modification guidance (typical for snoRNAs, but SNORD115 is orphan)Possible involvement in RNA editing (A-to-I editing of HTR2C)
03

Disease associations

Prader-Willi syndrome (SNORD115 deletions are common, may contribute to symptoms; mechanistic role remains debated)Neuropsychiatric disorders (potential relevance via HTR2C modulation, including anxiety, depression, and obsessive-compulsive behaviors, based on animal studies and association)

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