CACNA1F

Chr XX-linkedXLR

calcium voltage-gated channel subunit alpha1 F

Also known as: AIED, COD3, COD4, CORDX, CORDX3, CSNB2, CSNB2A, CSNBX2

This gene encodes the alpha-1F subunit of voltage-sensitive L-type calcium channels that mediate calcium influx into excitable cells, particularly important for neurotransmitter release and cellular signaling. Mutations cause X-linked eye disorders including congenital stationary night blindness type 2A, cone-rod dystrophy, and Aland Island eye disease. The gene shows X-linked recessive inheritance and is highly constrained against loss-of-function variants.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
LOFmechanismX-linked/XLRLOEUF 0.453 OMIM phenotypes
Clinical SummaryCACNA1F
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Gene-Disease Validity (ClinGen)
CACNA1F-related retinopathy · XLDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.32) despite low pLI — interpret in context.
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ClinVar Variants
74 unique Pathogenic / Likely Pathogenic· 253 VUS of 500 total submissions
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GeneReview available — CACNA1F
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.45LOEUF
pLI 0.000
Z-score 5.40
OE 0.32 (0.230.45)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
2.60Z-score
OE missense 0.75 (0.700.80)
632 obs / 844.7 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.32 (0.230.45)
00.351.4
Missense OE0.75 (0.700.80)
00.61.4
Synonymous OE0.89
01.21.6
LoF obs/exp: 23 / 72.7Missense obs/exp: 632 / 844.7Syn Z: 1.60
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveCACNA1F-related Aland Island eye diseaseLOFXLR
DN
0.79top 25%
GOF
0.85top 5%
LOF
0.2189th %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
DNprediction above median
LOF77% of P/LP variants are LoF · LOEUF 0.45

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. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

500 submitted variants in ClinVar

Classification Summary

Pathogenic50
Likely Pathogenic24
VUS253
Likely Benign135
Benign3
Conflicting1
50
Pathogenic
24
Likely Pathogenic
253
VUS
135
Likely Benign
3
Benign
1
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
36
1
13
0
50
Likely Pathogenic
21
2
1
0
24
VUS
6
228
17
2
253
Likely Benign
1
3
67
64
135
Benign
0
0
3
0
3
Conflicting
1
Total6423410166466

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

View in ClinVar →

Protein Context — Lollipop Plot

CACNA1F · 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 →
Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
PubTator3
Top 5 full-text resultsSearch PubTator3 ↗