ATP2B1

Chr 12AD

ATPase plasma membrane Ca2+ transporting 1

Also known as: MRD66, PMCA1, PMCA1kb

The ATP2B1 protein is a plasma membrane calcium ATPase that removes calcium ions from cells to maintain intracellular calcium homeostasis and regulate blood pressure through vascular smooth muscle function. Mutations cause autosomal dominant intellectual developmental disorder with onset typically in early development. This gene is extremely intolerant to loss-of-function variants (pLI >0.99), indicating that functional copies are essential for normal neurodevelopment.

OMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismADLOEUF 0.081 OMIM phenotype
Clinical SummaryATP2B1
Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 1.00). One damaged copy is likely sufficient to cause disease.
📋
ClinVar Variants
51 unique Pathogenic / Likely Pathogenic· 194 VUS of 286 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Dual constrained — LoF & missense intolerant
LoF Constraint
0.08LOEUF
pLI 1.000
Z-score 6.83
OE 0.02 (0.010.08)
Highly constrained

Among the most LoF-intolerant genes (~top 3%)

Missense Constraint
5.29Z-score
OE missense 0.42 (0.380.46)
271 obs / 650.9 exp
Constrained

Extremely missense-constrained (top ~0.01%)

Observed / Expected Ratios
LoF OE0.02 (0.010.08)
00.351.4
Missense OE0.42 (0.380.46)
00.61.4
Synonymous OE0.91
01.21.6
LoF obs/exp: 1 / 56.3Missense obs/exp: 271 / 650.9Syn Z: 1.05
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
moderateATP2B1-related neurodevelopmental disorderOTHERAD
DN
0.3693th %ile
GOF
0.6638th %ile
LOF
0.67top 25%

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

LOFprediction above median · 63% of P/LP variants are LoF · LOEUF 0.08
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

286 submitted variants in ClinVar

Classification Summary

Pathogenic24
Likely Pathogenic27
VUS194
Likely Benign11
Benign5
Conflicting3
24
Pathogenic
27
Likely Pathogenic
194
VUS
11
Likely Benign
5
Benign
3
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
15
1
8
0
24
Likely Pathogenic
17
9
1
0
27
VUS
0
185
7
2
194
Likely Benign
0
5
2
4
11
Benign
0
1
0
4
5
Conflicting
3
Total322011810264

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

View in ClinVar →

Protein Context — Lollipop Plot

ATP2B1 · 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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