KCNG2

Chr 18

potassium voltage-gated channel modifier subfamily G member 2

Also known as: KCNF2, KV6.2

The protein is a regulatory gamma subunit of voltage-gated potassium channels that modulates channel kinetics and voltage-dependent activation when coassembled with other subunits like KCNB1, contributing to cellular excitability regulation including cardiac action potential repolarization. Mutations in KCNG2 cause autosomal dominant epileptic encephalopathy with onset typically in early childhood. The gene shows moderate constraint against loss-of-function variants (LOEUF 0.67), suggesting some intolerance to complete protein loss.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
4
Pubs (1 yr)
165
P/LP submissions
0%
P/LP missense
0.67
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryKCNG2
Population Constraint (gnomAD)
Moderately constrained gene (pLI 0.60) — some intolerance to loss-of-function variants.
📋
ClinVar Variants
163 unique Pathogenic / Likely Pathogenic· 104 VUS of 279 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.67LOEUF
pLI 0.602
Z-score 2.13
OE 0.14 (0.050.67)
Moderately constrained

Typical tolerance to LoF variation

Missense Constraint
1.75Z-score
OE missense 0.70 (0.620.79)
185 obs / 265.0 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.14 (0.050.67)
00.351.4
Missense OE0.70 (0.620.79)
00.61.4
Synonymous OE1.06
01.21.6
LoF obs/exp: 1 / 7.1Missense obs/exp: 185 / 265.0Syn Z: -0.53
DN
0.7133th %ile
GOF
0.89top 5%
LOF
0.3259th %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

279 submitted variants in ClinVar

Classification Summary

Pathogenic156
Likely Pathogenic7
VUS104
Likely Benign10
156
Pathogenic
7
Likely Pathogenic
104
VUS
10
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
156
0
156
Likely Pathogenic
0
0
7
0
7
VUS
0
83
21
0
104
Likely Benign
0
2
6
2
10
Benign
0
0
0
0
0
Total0851902277

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

View in ClinVar →

Protein Context — Lollipop Plot

KCNG2 · 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.

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Clinical Literature
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Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC

No open access results found