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Small nucleolar RNA SNORD115-16 (SNORD115-16)

Target
SNORD115-16
Molecular classification
Small nucleolar RNA (snoRNA), Non-coding RNA, C/D box snoRNA, Guide RNA
01

Overview

Small nucleolar RNA SNORD115-16 (also known as HBII-52-16) is a member of the SNORD115 (HBII-52) family of C/D box small nucleolar RNAs, which are non-coding RNAs enriched in the nucleolus[1][4]. Unlike typical C/D box snoRNAs, which guide site-specific 2′-O-methylation of ribosomal or snRNAs, SNORD115-16 and its family members are considered "orphan" snoRNAs because they lack significant complementarity with rRNAs or snRNAs and do not direct canonical methylation[1][4]. Instead, they have a highly conserved antisense element that binds to the pre-mRNA of the serotonin receptor 2C (HTR2C) and regulate its alternative splicing[2][5][6]. This regulatory function influences the production and function of the 5-HT2C receptor isoforms, which in turn affect serotonergic signaling in the brain[2][6]. Loss of SNORD115 expression in the Prader–Willi syndrome region leads to brain-specific splicing defects and contributes to disease pathogenesis[3][4]. SNORD115-16 is repeated as part of a large tandem array in the human genome localized to chromosome 15q11–q13, a region critical in Prader–Willi and Angelman syndromes[4]. There is no evidence that SNORD115-16 is targeted by any drugs, used as a biomarker, or is itself a conventional "therapeutic target" such as a receptor, enzyme, or transporter[5]. Most research points to its function in RNA processing and brain-specific gene regulation, rather than a direct molecular target for small molecules or biologics.

Other names
HBII-52-16
02

Biological functions

Regulation of alternative splicing of target pre-mRNAs, especially serotonin receptor 2C (HTR2C) pre-mRNA[2][5][6]Possible base-pairing to target mRNAs to modulate exon inclusion[2][6]May modulate RNA editing (A-to-I editing inhibition) in the serotonin receptor 2C mRNA[4][6]Probable involvement in RNA processing in neuronal cells[6]
03

Disease associations

Implicated in Prader–Willi syndrome due to deletion or lack of expression in the 15q11–q13 region[3][4]Linked to neuronal dysfunction; possibly involved in the regulation of genes and splicing in brain tissue[3][4][6]

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