CHRNA4

Chr 20AD

cholinergic receptor nicotinic alpha 4 subunit

Also known as: BFNC, EBN, EBN1, NACHR, NACHRA4, NACRA4

This gene encodes the α4 subunit of neuronal nicotinic acetylcholine receptors, which are pentameric ligand-gated cation channels that mediate excitatory synaptic transmission in the central nervous system. Mutations cause autosomal dominant nocturnal frontal lobe epilepsy type 1, a seizure disorder typically beginning in childhood or adolescence with brief nocturnal seizures arising from the frontal lobe. The gene shows low constraint to loss-of-function variation (pLI = 0.00009, LOEUF = 0.822), consistent with autosomal dominant inheritance where heterozygous mutations are pathogenic.

OMIMResearchSummary from RefSeq, OMIM, UniProt
GOFmechanismADLOEUF 0.822 OMIM phenotypes
Clinical SummaryCHRNA4
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Gene-Disease Validity (ClinGen)
sleep-related hypermotor epilepsy · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.82LOEUF
pLI 0.000
Z-score 2.17
OE 0.48 (0.300.82)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.34Z-score
OE missense 0.95 (0.871.04)
377 obs / 396.1 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.48 (0.300.82)
00.351.4
Missense OE0.95 (0.871.04)
00.61.4
Synonymous OE1.22
01.21.6
LoF obs/exp: 10 / 20.6Missense obs/exp: 377 / 396.1Syn Z: -2.33
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveCHRNA4-related nocturnal frontal lobe epilepsyGOFAD
DN
0.83top 10%
GOF
0.84top 5%
LOF
0.2387th %ile

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function, dominant-negative and loss-of-function). 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
LOF1 literature citation

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

GOFIncreased dopamine release may result from a gain-of-function in nAChRs with the mutant CHRNA4 subunit, since nAChRs regulate dopamine release.PMID:18685138
LOFHaploinsufficiency for CHRNA4 and ARFGAP1 may have contributed towards a severe phenotype.PMID:17290276

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

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

CHRNA4 · 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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