ATP2A3

Chr 17

ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 3

Also known as: SERCA3

This gene encodes a SERCA calcium-ATPase that transports calcium ions from the cytosol into the sarcoplasmic/endoplasmic reticulum lumen, contributing to calcium sequestration during muscular excitation and contraction. Mutations cause cerebellar ataxia, areflexia, pes cavus, optic atrophy, and sensorineural hearing loss (CAPOS syndrome) and X-linked dystonia-parkinsonism, both following X-linked inheritance patterns. The gene is highly intolerant to loss-of-function mutations, and the associated disorders primarily affect the nervous system with movement abnormalities and sensory deficits.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 0.66
Clinical SummaryATP2A3
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
26 unique Pathogenic / Likely Pathogenic· 143 VUS of 246 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.66LOEUF
pLI 0.000
Z-score 3.51
OE 0.46 (0.330.66)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
1.83Z-score
OE missense 0.80 (0.740.86)
537 obs / 670.5 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.46 (0.330.66)
00.351.4
Missense OE0.80 (0.740.86)
00.61.4
Synonymous OE1.19
01.21.6
LoF obs/exp: 23 / 49.7Missense obs/exp: 537 / 670.5Syn Z: -2.53
DN
0.78top 25%
GOF
0.82top 10%
LOF
0.2092th %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

246 submitted variants in ClinVar

Classification Summary

Pathogenic26
VUS143
Likely Benign36
Benign25
Conflicting2
26
Pathogenic
143
VUS
36
Likely Benign
25
Benign
2
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
26
0
26
Likely Pathogenic
0
0
0
0
0
VUS
0
132
11
0
143
Likely Benign
0
7
6
23
36
Benign
0
4
3
18
25
Conflicting
2
Total01434641232

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

View in ClinVar →

Protein Context — Lollipop Plot

ATP2A3 · 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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