SNURF

Chr 15

SNRPN upstream open reading frame

SNURF encodes an E3 ubiquitin-protein ligase that targets polysumoylated proteins for proteasomal degradation and regulates chromosome alignment, spindle assembly, and cellular responses to stress. Loss of SNURF expression due to paternal deletions or imprinting defects in the chromosome 15q11-q13 region causes Prader-Willi syndrome, characterized by neonatal hypotonia, feeding difficulties, and later-onset hyperphagia and obesity. The gene shows paternal-only expression due to genomic imprinting, so only paternal genetic alterations result in disease.

OMIMResearchSummary from RefSeq, UniProt
GOFmechanism

Population Genetics & Constraint

Constraint data not available from gnomAD.

DN
0.5379th %ile
GOF
0.74top 25%
LOF
0.3162th %ile

The highest-scoring mechanism for this gene is gain-of-function.

GOFprediction above median

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

SNURF · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

Search ClinicalTrials.gov →
Clinical Literature
Open Research Assistant →