GPM6A

Chr 4

glycoprotein M6A

Also known as: GPM6, M6A

The protein functions in neuronal differentiation and migration, neurite outgrowth, and synaptic plasticity through calcium channel activity and MAPK signaling pathways. Mutations cause neurodevelopmental disorders with intellectual disability and developmental delays, typically with autosomal dominant inheritance. The gene is highly constrained against loss-of-function variants (pLI 0.99, LOEUF 0.22), indicating intolerance to protein-truncating mutations.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
11
Pubs (1 yr)
76
P/LP submissions
P/LP missense
0.22
LOEUF· LoF intol.
Multiple*
Mechanism· predicted
Clinical SummaryGPM6A
Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 0.99). One damaged copy is likely sufficient to cause disease.
📋
ClinVar Variants
76 unique Pathogenic / Likely Pathogenic· 16 VUS of 105 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.22LOEUF
pLI 0.990
Z-score 3.43
OE 0.00 (0.000.22)
Highly constrained

Highly LoF-intolerant (top ~10% of genes)

Missense Constraint
1.96Z-score
OE missense 0.56 (0.470.67)
89 obs / 158.6 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.00 (0.000.22)
00.351.4
Missense OE0.56 (0.470.67)
00.61.4
Synonymous OE1.00
01.21.6
LoF obs/exp: 0 / 13.7Missense obs/exp: 89 / 158.6Syn Z: 0.00
DN
0.4685th %ile
GOF
0.75top 25%
LOF
0.52top 25%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and gain-of-function). The Badonyi & Marsh model scores gain-of-function highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports loss-of-function (haploinsufficiency). Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

LOFLOEUF 0.22
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. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

105 submitted variants in ClinVar

Classification Summary

Pathogenic74
Likely Pathogenic2
VUS16
Likely Benign1
74
Pathogenic
2
Likely Pathogenic
16
VUS
1
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories· variant type breakdown unavailable

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
74
Likely Pathogenic
2
VUS
16
Likely Benign
1
Benign
0
Total93

Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

GPM6A · 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.

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Clinical Literature
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