GPR173

Chr X

G protein-coupled receptor 173

Also known as: SREB3

The protein is a G-protein coupled receptor that responds to phoenixin peptides and mediates their effects on gonadotropin-releasing hormone signaling in the hypothalamus and pituitary, as well as granulosa cell proliferation in the ovary. Mutations in this gene have been associated with hypogonadotropic hypogonadism, which involves impaired reproductive hormone function. The gene is highly constrained against loss-of-function variants (pLI = 0.87), suggesting that complete loss of protein function is poorly tolerated.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 0.44
Clinical SummaryGPR173
Population Constraint (gnomAD)
Moderately constrained gene (pLI 0.87) — some intolerance to loss-of-function variants.
📋
ClinVar Variants
61 unique Pathogenic / Likely Pathogenic· 27 VUS of 100 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.44LOEUF
pLI 0.874
Z-score 2.41
OE 0.00 (0.000.44)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
2.26Z-score
OE missense 0.53 (0.440.62)
95 obs / 180.7 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.00 (0.000.44)
00.351.4
Missense OE0.53 (0.440.62)
00.61.4
Synonymous OE0.90
01.21.6
LoF obs/exp: 0 / 6.8Missense obs/exp: 95 / 180.7Syn Z: 0.68
DN
0.4190th %ile
GOF
0.6832th %ile
LOF
0.61top 25%

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function and loss-of-function). 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
LOFLOEUF 0.44

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. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

100 submitted variants in ClinVar

Classification Summary

Pathogenic57
Likely Pathogenic4
VUS27
Conflicting1
57
Pathogenic
4
Likely Pathogenic
27
VUS
1
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
57
0
57
Likely Pathogenic
0
0
4
0
4
VUS
0
24
3
0
27
Likely Benign
0
0
0
0
0
Benign
0
0
0
0
0
Conflicting
1
Total02464089

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

View in ClinVar →

Protein Context — Lollipop Plot

GPR173 · 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 →
Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
PubTator3
Top 5 full-text resultsSearch PubTator3 ↗