GPSM1

Chr 9

G protein signaling modulator 1

Also known as: AGS3

The protein functions as a guanine nucleotide dissociation inhibitor that keeps G(i/o) alpha subunits in their GDP-bound state and controls spindle orientation and asymmetric cell fate in cerebral cortical progenitors. Mutations cause autosomal recessive Chudley-McCullough syndrome, characterized by early-onset sensorineural hearing loss and brain malformations including polymicrogyria and cerebellar hypoplasia. The gene is highly intolerant to loss-of-function variants, indicating that complete loss of protein function is likely pathogenic.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 0.68
Clinical SummaryGPSM1
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
72 unique Pathogenic / Likely Pathogenic· 155 VUS of 253 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.68LOEUF
pLI 0.000
Z-score 2.90
OE 0.43 (0.280.68)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.39Z-score
OE missense 0.95 (0.871.03)
420 obs / 443.4 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.43 (0.280.68)
00.351.4
Missense OE0.95 (0.871.03)
00.61.4
Synonymous OE0.99
01.21.6
LoF obs/exp: 13 / 30.2Missense obs/exp: 420 / 443.4Syn Z: 0.15
DN
0.74top 25%
GOF
0.81top 10%
LOF
0.2873th %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

253 submitted variants in ClinVar

Classification Summary

Pathogenic69
Likely Pathogenic3
VUS155
Likely Benign4
Conflicting2
69
Pathogenic
3
Likely Pathogenic
155
VUS
4
Likely Benign
2
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
69
0
69
Likely Pathogenic
0
0
3
0
3
VUS
0
145
10
0
155
Likely Benign
0
2
1
1
4
Benign
0
0
0
0
0
Conflicting
2
Total0147831233

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

View in ClinVar →

Protein Context — Lollipop Plot

GPSM1 · 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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