KCNC2

Chr 12

potassium voltage-gated channel subfamily C member 2

Also known as: DEE103, KV3.2

The protein forms voltage-gated potassium channels that mediate fast action potential repolarization and enable sustained high-frequency firing in central nervous system neurons, particularly in GABAergic interneurons and cells involved in gamma oscillations. Mutations cause developmental and epileptic encephalopathy 103 through an autosomal dominant inheritance pattern via a gain-of-function mechanism. The altered channel function disrupts neuronal excitability and synaptic transmission, leading to seizures and developmental impairment.

GeneReviewsResearchSummary from RefSeq, OMIM, UniProt, Mechanism
MultiplemechanismLOEUF 0.53
Clinical SummaryKCNC2
🧬
Gene-Disease Validity (ClinGen)
developmental and epileptic encephalopathy · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.25) despite low pLI — interpret in context.
📖
GeneReview available — KCNC2
Authoritative clinical overview · Recommended first read
Open GeneReview ↗
Some data sources returned errors (1)

omim: Error: OMIM fetch failed: 429

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.53LOEUF
pLI 0.189
Z-score 3.07
OE 0.25 (0.130.53)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
2.98Z-score
OE missense 0.56 (0.500.63)
204 obs / 363.7 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.25 (0.130.53)
00.351.4
Missense OE0.56 (0.500.63)
00.61.4
Synonymous OE1.20
01.21.6
LoF obs/exp: 5 / 19.7Missense obs/exp: 204 / 363.7Syn Z: -2.01
DN
0.79top 25%
GOF
0.85top 5%
LOF
0.3454th %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 · 1 literature citation
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.

Literature Evidence

GOFFunctional analysis of 4 variants demonstrated gain of function in 3 severely affected DEE cases and loss of function in 1 case with a milder phenotype (GGE) as the underlying pathomechanisms.DISCUSSION: These findings implicate KCNC2 as a novel causative gene for epilepsy and emphasize the criticalPMID:35314505

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

KCNC2 · 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
Open Research Assistant →
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC