CHRNB1

Chr 17ARAD

cholinergic receptor nicotinic beta 1 subunit

Also known as: ACHRB, CHRNB, CMS1D, CMS2A, CMS2C, SCCMS

This gene encodes the beta subunit of the muscle acetylcholine receptor, which opens an ion channel across the postsynaptic membrane when acetylcholine binds. Mutations cause congenital myasthenic syndrome with either slow-channel kinetics (autosomal dominant, gain-of-function mechanism) or acetylcholine receptor deficiency (autosomal recessive). The dominant form results from prolonged channel opening, while the recessive form involves receptor deficiency.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
MultiplemechanismAR/ADLOEUF 1.002 OMIM phenotypes
Clinical SummaryCHRNB1
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Gene-Disease Validity (ClinGen)
congenital myasthenic syndrome 2C · ARDefinitive

Definitive — sufficient evidence for diagnostic panels

2 total gene-disease associations curated

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
24 unique Pathogenic / Likely Pathogenic· 168 VUS of 300 total submissions
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GeneReview available — CHRNB1
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.00LOEUF
pLI 0.000
Z-score 1.58
OE 0.65 (0.431.00)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.44Z-score
OE missense 0.93 (0.841.03)
266 obs / 286.9 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.65 (0.431.00)
00.351.4
Missense OE0.93 (0.841.03)
00.61.4
Synonymous OE1.02
01.21.6
LoF obs/exp: 15 / 23.2Missense obs/exp: 266 / 286.9Syn Z: -0.19
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveCHRNB1-related congenital myaestheniaLOFAR
definitiveCHRNB1-related congenital myaestheniaGOFAD
DN
0.80top 10%
GOF
0.83top 10%
LOF
0.1896th %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 · 1 literature citation
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.

Literature Evidence

GOFThe pronounced abnormalities in neuromuscular synaptic architecture and function, muscle fiber damage and weakness, resulting from a single point mutation are a dramatic example of a mutation having a dominant gain of function and of hereditary excitotoxicity.PMID:8651643

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

ClinVar Variant Classifications

300 submitted variants in ClinVar

Classification Summary

Pathogenic16
Likely Pathogenic8
VUS168
Likely Benign93
Benign2
Conflicting4
16
Pathogenic
8
Likely Pathogenic
168
VUS
93
Likely Benign
2
Benign
4
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
4
0
12
0
16
Likely Pathogenic
8
0
0
0
8
VUS
5
148
11
4
168
Likely Benign
0
1
42
50
93
Benign
0
0
2
0
2
Conflicting
4
Total171496754291

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

View in ClinVar →

Protein Context — Lollipop Plot

CHRNB1 · 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
Open Research Assistant →