OPRL1

Chr 20

opioid related nociceptin receptor 1

Also known as: KOR-3, KOR3, NOCIR, NOP, NOPr, OOR, OPRL, ORL1

The protein is a G-protein coupled receptor that binds the neuropeptide nociceptin and modulates pain perception, locomotor activity, stress responses, and learning and memory through inhibition of adenylate cyclase and calcium channel activity. The gene shows moderate constraint against loss-of-function variants (LOEUF 0.617), but no established human disease associations with OPRL1 mutations are currently documented in the provided data. This receptor system represents a potential therapeutic target for pain and neuropsychiatric conditions, though its role in pediatric neurogenetic disorders remains to be established.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
10
Pubs (1 yr)
37
P/LP submissions
0%
P/LP missense
0.62
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryOPRL1
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.20) despite low pLI — interpret in context.
📋
ClinVar Variants
37 unique Pathogenic / Likely Pathogenic· 105 VUS of 153 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.62LOEUF
pLI 0.482
Z-score 2.38
OE 0.20 (0.080.62)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
1.41Z-score
OE missense 0.75 (0.660.84)
187 obs / 249.9 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.20 (0.080.62)
00.351.4
Missense OE0.75 (0.660.84)
00.61.4
Synonymous OE1.00
01.21.6
LoF obs/exp: 2 / 10.2Missense obs/exp: 187 / 249.9Syn Z: 0.01
DN
0.7325th %ile
GOF
0.84top 5%
LOF
0.2969th %ile

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function and dominant-negative). Both the Badonyi & Marsh prediction and the broader genomic evidence point to gain-of-function as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

GOFprediction above median
DNprediction 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

153 submitted variants in ClinVar

Classification Summary

Pathogenic30
Likely Pathogenic7
VUS105
Likely Benign3
Benign4
30
Pathogenic
7
Likely Pathogenic
105
VUS
3
Likely Benign
4
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
30
0
30
Likely Pathogenic
0
0
7
0
7
VUS
0
96
9
0
105
Likely Benign
0
3
0
0
3
Benign
0
0
1
3
4
Total099473149

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

OPRL1 · 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
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