KCNA6

Chr 12

potassium voltage-gated channel subfamily A member 6

Also known as: HBK2, KV1.6, PPP1R96

KCNA6 encodes a voltage-gated potassium channel that forms tetrameric channels regulating potassium transport and neuronal excitability in the nervous system. Mutations cause early infantile epileptic encephalopathy with developmental delay, seizures, and intellectual disability, following an autosomal dominant inheritance pattern. The gene shows moderate constraint against loss-of-function variants (LOEUF 0.526), and the associated epileptic encephalopathy typically presents in infancy.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 0.53
Clinical SummaryKCNA6
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.20) despite low pLI — interpret in context.
📋
ClinVar Variants
60 unique Pathogenic / Likely Pathogenic· 85 VUS of 153 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.53LOEUF
pLI 0.497
Z-score 2.84
OE 0.20 (0.090.53)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
3.05Z-score
OE missense 0.53 (0.470.60)
180 obs / 337.6 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.20 (0.090.53)
00.351.4
Missense OE0.53 (0.470.60)
00.61.4
Synonymous OE0.97
01.21.6
LoF obs/exp: 3 / 14.8Missense obs/exp: 180 / 337.6Syn Z: 0.32
DN
0.74top 25%
GOF
0.82top 10%
LOF
0.3452th %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

153 submitted variants in ClinVar

Classification Summary

Pathogenic54
Likely Pathogenic6
VUS85
Likely Benign2
54
Pathogenic
6
Likely Pathogenic
85
VUS
2
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
2
52
0
54
Likely Pathogenic
0
1
5
0
6
VUS
1
75
9
0
85
Likely Benign
0
2
0
0
2
Benign
0
0
0
0
0
Total180660147

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

View in ClinVar →

Protein Context — Lollipop Plot

KCNA6 · 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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