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・ Small nucleolar RNA SNORA75
・ Small nucleolar RNA SNORA76
・ Small nucleolar RNA SNORA77
・ Small nucleolar RNA SNORA79
・ Small nucleolar RNA SNORA8
・ Small nucleolar RNA SNORA9
・ Small nucleolar RNA SNORD100
・ Small nucleolar RNA SNORD101
・ Small nucleolar RNA SNORD102
・ Small nucleolar RNA SNORD103
・ Small nucleolar RNA SNORD105
・ Small nucleolar RNA SNORD110
・ Small nucleolar RNA SNORD111
・ Small nucleolar RNA SNORD113
・ Small nucleolar RNA SNORD115
Small nucleolar RNA SNORD116
・ Small nucleolar RNA SNORD14
・ Small nucleolar RNA SNORD15
・ Small nucleolar RNA SNORD16
・ Small nucleolar RNA SNORD17
・ Small nucleolar RNA SNORD18
・ Small nucleolar RNA SNORD19
・ Small nucleolar RNA SNORD20
・ Small nucleolar RNA SNORD21
・ Small nucleolar RNA SNORD22
・ Small nucleolar RNA SNORD23
・ Small nucleolar RNA SNORD24
・ Small nucleolar RNA SNORD25
・ Small nucleolar RNA SNORD26
・ Small nucleolar RNA SNORD27


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Small nucleolar RNA SNORD116 : ウィキペディア英語版
Small nucleolar RNA SNORD116

SNORD116 (also known as HBII-85) is a non-coding RNA (ncRNA) molecule which functions in the modification of other small nuclear RNAs (snRNAs). This type of modifying RNA is usually located in the nucleolus of the eukaryotic cell which is a major site of snRNA biogenesis. It is known as a small nucleolar RNA (snoRNA) and also often referred to as a guide RNA.
SNORD116 belongs to the C/D box class of snoRNAs which contain the conserved sequence motifs known as the C box (UGAUGA) and the D box (CUGA). Most of the members of the box C/D family function in directing site-specific 2'-O-methylation of substrate RNAs.
In the human genome, there are 29 tandemnly repeated copies of SNORD116, followed by 48 copies of another C/D box snoRNA, SNORD115, in the Prader-Willi syndrome (PWS) region of chromosome 15. Unlike most other snoRNAs, SNORD116 is expressed prevalently in the brain (but is absent in PWS patients) and lacks any significant complementarity with ribosomal RNA. Mouse models of PWS show similar symptoms to humans (hyperphagia and growth deficiency), providing further evidence that PWS is directly linked to the deletion of SNORD116.
More evidence comes from the discovery of two individuals that share many traits of PWS sufferers, both have atypical microdeletions on chromosome 15q11-13, the intersection of which contains only the SNORD116 snoRNAs. An early paper, however, disputes these findings.
The targets of SNORD116 are unknown, however a bioinformatic screen located 23 possible targets within protein coding genes, of these a large fraction were found to be alternatively spliced, suggesting a role of SNORD116 in the regulation of alternative splicing.
==References==



抄文引用元・出典: フリー百科事典『 ウィキペディア(Wikipedia)
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