KCNB2

Chr 8

potassium voltage-gated channel subfamily B member 2

Also known as: KV2.2

The KCNB2 protein forms voltage-gated potassium channels that regulate neuronal excitability and transmembrane potassium transport, functioning as delayed-rectifier channels primarily in brain and smooth muscle cells. Mutations cause autosomal dominant epileptic encephalopathy with developmental delay and intellectual disability, typically presenting in early childhood. This gene is highly constrained against loss-of-function mutations, indicating that KCNB2 variants are likely to have significant clinical impact.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 0.26
Clinical SummaryKCNB2
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.

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.26LOEUF
pLI 0.996
Z-score 4.53
OE 0.10 (0.040.26)
Highly constrained

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

Missense Constraint
2.25Z-score
OE missense 0.72 (0.660.79)
368 obs / 511.2 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.10 (0.040.26)
00.351.4
Missense OE0.72 (0.660.79)
00.61.4
Synonymous OE1.11
01.21.6
LoF obs/exp: 3 / 29.6Missense obs/exp: 368 / 511.2Syn Z: -1.34
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
moderateKCNB2-related neurodevelopmental disorderOTHERAD
DN
0.5576th %ile
GOF
0.75top 25%
LOF
0.60top 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 0.26
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

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

KCNB2 · 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.

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Clinical Literature
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