KCNH4

Chr 17

potassium voltage-gated channel subfamily H member 4

Also known as: BEC2, ELK1, Kv12.3

The protein forms the pore-forming alpha subunit of voltage-gated delayed rectifier potassium channels that regulate neuronal excitability in the neocortex and striatum. Mutations cause autosomal dominant epilepsy through a gain-of-function mechanism, where altered channel properties disrupt normal neuronal firing patterns. The gene is highly intolerant to loss-of-function variants, consistent with the pathogenic mechanism being gain-of-function rather than haploinsufficiency.

Summary from RefSeq, UniProt, Mechanism
0
Active trials
1
Pubs (1 yr)
6
P/LP submissions
0%
P/LP missense
0.21
LOEUF· LoF intol.
GOF
Mechanism· predicted
Clinical SummaryKCNH4
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
6 unique Pathogenic / Likely Pathogenic· 123 VUS of 141 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.21LOEUF
pLI 1.000
Z-score 5.48
OE 0.09 (0.040.21)
Highly constrained

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

Missense Constraint
2.94Z-score
OE missense 0.67 (0.620.73)
435 obs / 645.3 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.09 (0.040.21)
00.351.4
Missense OE0.67 (0.620.73)
00.61.4
Synonymous OE0.96
01.21.6
LoF obs/exp: 4 / 42.6Missense obs/exp: 435 / 645.3Syn Z: 0.56
DN
0.6064th %ile
GOF
0.77top 25%
LOF
0.58top 25%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and gain-of-function). The Badonyi & Marsh model scores gain-of-function highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports loss-of-function (haploinsufficiency). Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

LOFLOEUF 0.21
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

141 submitted variants in ClinVar

Classification Summary

Pathogenic6
VUS123
Likely Benign6
Benign1
6
Pathogenic
123
VUS
6
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
6
0
6
Likely Pathogenic
0
0
0
0
0
VUS
1
121
1
0
123
Likely Benign
0
3
0
3
6
Benign
0
0
0
1
1
Total112474136

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

View in ClinVar →

Protein Context — Lollipop Plot

KCNH4 · 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
Open Research Assistant →
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC

No open access results found