KCND2

Chr 7

potassium voltage-gated channel subfamily D member 2

Also known as: KV4.2, RK5

The protein forms voltage-gated potassium channels that regulate neuronal excitability by mediating A-type potassium currents, particularly important for controlling action potential firing patterns and back-propagation in brain neurons. Mutations cause autosomal dominant epileptic encephalopathy, early infantile, and seizures, benign familial infantile, affecting neuronal excitability and seizure threshold. This gene shows moderate constraint against loss-of-function variants (LOEUF 0.574) and has an established GeneReviews entry indicating clinical significance.

GeneReviewsOMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 0.57
Clinical SummaryKCND2
🧬
Gene-Disease Validity (ClinGen)
KCND2-related neurodevelopmental disorder with or without seizures · ADModerate

Moderate evidence — consider for supplementary testing

Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.32) despite low pLI — interpret in context.
📋
ClinVar Variants
27 unique Pathogenic / Likely Pathogenic· 209 VUS of 414 total submissions
📖
GeneReview available — KCND2
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Missense constrained — critical functional residues
LoF Constraint
0.57LOEUF
pLI 0.012
Z-score 3.17
OE 0.32 (0.190.57)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
3.51Z-score
OE missense 0.49 (0.440.56)
189 obs / 382.3 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.32 (0.190.57)
00.351.4
Missense OE0.49 (0.440.56)
00.61.4
Synonymous OE0.95
01.21.6
LoF obs/exp: 8 / 25.1Missense obs/exp: 189 / 382.3Syn Z: 0.45
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
moderateKCND2-related neurodevelopmental disorder with or without seizuresOTHERAD
DN
0.81top 10%
GOF
0.82top 10%
LOF
0.2775th %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

414 submitted variants in ClinVar

Classification Summary

Pathogenic21
Likely Pathogenic6
VUS209
Likely Benign153
Benign20
Conflicting5
21
Pathogenic
6
Likely Pathogenic
209
VUS
153
Likely Benign
20
Benign
5
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
3
18
0
21
Likely Pathogenic
0
5
1
0
6
VUS
13
176
17
3
209
Likely Benign
0
9
28
116
153
Benign
0
1
14
5
20
Conflicting
5
Total1319478124414

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

View in ClinVar →

Protein Context — Lollipop Plot

KCND2 · 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 →