AQP4

Chr 18AR

aquaporin 4

Also known as: MIWC, MLC4, WCH4, hAQP4

This gene encodes aquaporin-4, a water-specific channel protein that maintains brain water homeostasis and facilitates glymphatic solute transport, including clearance of beta-amyloid peptides from brain interstitial fluid. Autosomal recessive mutations cause megalencephalic leukoencephalopathy with subcortical cysts 4, a remitting form of this white matter disorder. The gene shows minimal constraint against loss-of-function variants (pLI 0.002, LOEUF 0.99), consistent with recessive inheritance where heterozygous carriers are typically unaffected.

Summary from RefSeq, OMIM, UniProt
Research Assistant →

Primary Disease Associations & Inheritance

?Megalencephalic leukoencephalopathy with subcortical cysts 4, remittingMIM #620448
AR
5
Active trials
644
Pubs (1 yr)
39
P/LP submissions
5%
P/LP missense
0.99
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryAQP4
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
37 unique Pathogenic / Likely Pathogenic· 42 VUS of 96 total submissions
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Clinical Trials
5 active or recruiting trials — potential therapeutic options may be available
📖
GeneReview available — AQP4
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.99LOEUF
pLI 0.002
Z-score 1.59
OE 0.50 (0.270.99)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
-0.19Z-score
OE missense 1.04 (0.921.18)
187 obs / 179.7 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.50 (0.270.99)
00.351.4
Missense OE1.04 (0.921.18)
00.61.4
Synonymous OE1.10
01.21.6
LoF obs/exp: 6 / 11.9Missense obs/exp: 187 / 179.7Syn Z: -0.64
DN
0.87top 5%
GOF
0.88top 5%
LOF
0.1796th %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

96 submitted variants in ClinVar

Classification Summary

Pathogenic35
Likely Pathogenic2
VUS42
Likely Benign6
Benign5
Conflicting1
35
Pathogenic
2
Likely Pathogenic
42
VUS
6
Likely Benign
5
Benign
1
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
1
34
0
35
Likely Pathogenic
0
1
1
0
2
VUS
0
36
6
0
42
Likely Benign
0
5
1
0
6
Benign
0
1
0
4
5
Conflicting
1
Total04442491

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

View in ClinVar →

Protein Context — Lollipop Plot

AQP4 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold
Clinical Literature
Open Research Assistant →
Key Publications
Landmark & review papers · by relevance
PubMed
Top 5 results · since 2015Search PubMed ↗