CACNA1G

Chr 17AD

calcium voltage-gated channel subunit alpha1 G

Also known as: Ca(V)T.1, Cav3.1, NBR13, SCA42, SCA42ND

This gene encodes the alpha-1G subunit of T-type voltage-gated calcium channels, which generate low-threshold calcium currents essential for neuronal pacemaking, oscillations, and burst firing patterns. Mutations cause spinocerebellar ataxia 42 through an autosomal dominant inheritance pattern, with early-onset variants associated with severe neurodevelopmental deficits. The gene is highly constrained against loss-of-function variants, and mutations can cause disease predominantly through gain-of-function mechanisms that likely disrupt normal neuronal calcium signaling.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
GOFmechanismADLOEUF 0.212 OMIM phenotypes
Clinical SummaryCACNA1G
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Gene-Disease Validity (ClinGen)
spinocerebellar ataxia type 42 · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

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.
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GeneReview available — CACNA1G
Authoritative clinical overview · Recommended first read
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Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Dual constrained — LoF & missense intolerant
LoF Constraint
0.21LOEUF
pLI 1.000
Z-score 7.95
OE 0.13 (0.090.21)
Highly constrained

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

Missense Constraint
4.64Z-score
OE missense 0.66 (0.620.69)
963 obs / 1462.1 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.13 (0.090.21)
00.351.4
Missense OE0.66 (0.620.69)
00.61.4
Synonymous OE0.95
01.21.6
LoF obs/exp: 13 / 97.9Missense obs/exp: 963 / 1462.1Syn Z: 0.98
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
strongCACNA1G-related developmental disorder with hypotonia, epilepsy, and cerebral/cerebellar atrophyLOFAD
limitedCACNA1G-related intellectual developmental disorderLOFAR
Mechanism Note (expert annotation)
GOF

Cav3.1 (T-type) alpha subunit. Monoallelic pathogenic variants cause GOF with shifted voltage dependence and increased window current. G2P classifies as LOF, but electrophysiology data demonstrate gain-of-function at the channel level.

References:PMID:26586654
DN
0.5575th %ile
GOF
0.76top 25%
LOF
0.55top 25%

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function 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
LOFLOEUF 0.21

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

GOFEarly-onset severe spinocerebellar ataxia 42 with neurodevelopmental deficits (SCA42ND, MIM#604065) is an ultrarare autosomal dominant syndrome related to de novo CACNA1G gain-of-function pathogenic variants.PMID:33098379

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

CACNA1G · 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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Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC