GABRG2

Chr 5AD

gamma-aminobutyric acid type A receptor subunit gamma2

The gene encodes the gamma-2 subunit of GABA-A receptors, which are pentameric ligand-gated chloride channels that mediate inhibitory neurotransmission in the brain. Mutations cause autosomal dominant epilepsy syndromes including developmental and epileptic encephalopathy, generalized epilepsy with febrile seizures plus, and familial febrile seizures. Disease can result from multiple mechanisms depending on the specific variant, with some mutations causing loss of receptor function while others may produce dominant-negative or gain-of-function effects.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
GOF/LOFmechanismADLOEUF 0.403 OMIM phenotypes
Clinical SummaryGABRG2
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Gene-Disease Validity (ClinGen)
epilepsy · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Moderately constrained gene (pLI 0.74) — some intolerance to loss-of-function variants.
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Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available
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GeneReview available — GABRG2
Authoritative clinical overview · Recommended first read
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Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.40LOEUF
pLI 0.739
Z-score 3.86
OE 0.19 (0.100.40)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
2.99Z-score
OE missense 0.49 (0.430.57)
137 obs / 277.3 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.19 (0.100.40)
00.351.4
Missense OE0.49 (0.430.57)
00.61.4
Synonymous OE1.10
01.21.6
LoF obs/exp: 5 / 26.4Missense obs/exp: 137 / 277.3Syn Z: -0.79
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
strongGABRG2-related epilepsy, generalized, with febrile seizures plusLOFAD
Mechanism Note (variant-dependent)
LOFDN— mechanism depends on specific variant

GABA-A receptor gamma-2 subunit forms pentameric channels. Most pathogenic truncating mutations produce stable mutant proteins with dominant-negative effects on channel assembly. Missense variants reduce surface expression or channel function (LOF). Both LOF and DN mechanisms are established; GOF is not the primary mechanism despite Badonyi prediction.

DN
0.7131th %ile
GOF
0.73top 25%
LOF
0.4233th %ile

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative 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 dominant-negative. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

DNprediction above median · 1 literature citation
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.

Literature Evidence

DNMost GABRG2 truncating mutations associated with Dravet syndrome result in premature termination codons (PTCs) and are stably translated into mutant proteins with potential dominant-negative effects.PMID:24480790

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

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

GABRG2 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold
Clinical Literature
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