SV2A

Chr 1AR

synaptic vesicle glycoprotein 2A

Also known as: DEE113, SLC22B1, SV2

SV2A encodes a synaptic vesicle protein that enhances low-frequency neurotransmission by maintaining the readily releasable pool of secretory vesicles and positively regulating vesicle fusion. Autosomal recessive mutations cause developmental and epileptic encephalopathy 113, typically presenting in early childhood. The gene shows moderate constraint against loss-of-function variants (LOEUF 0.414), suggesting some tolerance to heterozygous loss.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismARLOEUF 0.411 OMIM phenotype
Clinical SummarySV2A
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.24) despite low pLI — interpret in context.
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ClinVar Variants
14 unique Pathogenic / Likely Pathogenic· 83 VUS of 130 total submissions
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Clinical Trials
5 active or recruiting trials — potential therapeutic options may be available
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GeneReview available — SV2A
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.41LOEUF
pLI 0.228
Z-score 4.36
OE 0.24 (0.140.41)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
2.12Z-score
OE missense 0.72 (0.660.79)
328 obs / 455.0 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.24 (0.140.41)
00.351.4
Missense OE0.72 (0.660.79)
00.61.4
Synonymous OE0.98
01.21.6
LoF obs/exp: 9 / 38.0Missense obs/exp: 328 / 455.0Syn Z: 0.20
DN
0.6646th %ile
GOF
0.73top 25%
LOF
0.2969th %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
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.

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

ClinVar Variant Classifications

130 submitted variants in ClinVar

Classification Summary

Pathogenic12
Likely Pathogenic2
VUS83
Likely Benign16
Benign5
12
Pathogenic
2
Likely Pathogenic
83
VUS
16
Likely Benign
5
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
1
0
11
0
12
Likely Pathogenic
2
0
0
0
2
VUS
1
77
4
1
83
Likely Benign
0
3
0
13
16
Benign
0
0
0
5
5
Total4801519118

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

View in ClinVar →

Protein Context — Lollipop Plot

SV2A · 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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