KCNA4

Chr 11AR

potassium voltage-gated channel subfamily A member 4

Also known as: HBK4, HK1, HPCN2, HUKII, KCNA4L, KCNA8, KV1.4, MCIDDS

KCNA4 encodes a voltage-gated potassium channel that mediates potassium transport in excitable membranes and can form homotetrameric or heterotetrameric channels with other KCNA family members. Autosomal recessive mutations cause a neurodevelopmental disorder characterized by microcephaly, cataracts, intellectual disability, and dystonia with striatal abnormalities. The gene is highly constrained against loss-of-function variants (pLI = 0.98, LOEUF = 0.28), indicating intolerance to functional disruption.

Summary from RefSeq, OMIM, UniProt
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Primary Disease Associations & Inheritance

Microcephaly, cataracts, impaired intellectual development, and dystonia with abnormal striatumMIM #618284
AR
0
Active trials
3
Pubs (1 yr)
22
P/LP submissions
0%
P/LP missense
0.28
LOEUF· LoF intol.
Multiple*
Mechanism· predicted
Clinical SummaryKCNA4
Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 0.98). One damaged copy is likely sufficient to cause disease.
📋
ClinVar Variants
22 unique Pathogenic / Likely Pathogenic· 74 VUS of 105 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.28LOEUF
pLI 0.983
Z-score 3.58
OE 0.06 (0.020.28)
Highly constrained

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

Missense Constraint
2.03Z-score
OE missense 0.71 (0.640.78)
267 obs / 377.8 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.06 (0.020.28)
00.351.4
Missense OE0.71 (0.640.78)
00.61.4
Synonymous OE1.16
01.21.6
LoF obs/exp: 1 / 16.9Missense obs/exp: 267 / 377.8Syn Z: -1.55
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
limitedKCNA4-related abnormal striatum, congenital cataract and intellectual disabilityOTHERAR

Predictions shown for reference only — model trained on dominant genes, not applicable to AR conditions.

DN
0.5870th %ile
GOF
0.6736th %ile
LOF
0.57top 25%

The Badonyi & Marsh prediction model was trained exclusively on dominant disease genes. Predictions are not reliable for genes with autosomal recessive inheritance and are shown at reduced opacity for reference only.

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

Pathogenic22
VUS74
Likely Benign6
Benign1
22
Pathogenic
74
VUS
6
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
22
0
22
Likely Pathogenic
0
0
0
0
0
VUS
0
72
2
0
74
Likely Benign
0
1
0
5
6
Benign
0
0
0
1
1
Total073246103

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

View in ClinVar →

Protein Context — Lollipop Plot

KCNA4 · protein map & ClinVar variants

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

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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