NOVA2

Chr 19AD

NOVA alternative splicing regulator 2

Also known as: ANOVA, NEDASB, NOVA-2, NOVA3

The NOVA2 protein regulates alternative splicing in neurons by binding to specific pre-mRNA sequences to control exon inclusion or exclusion, playing essential roles in cortical development, neural network wiring, and synapse formation. Mutations cause neurodevelopmental disorder with or without autistic features and/or structural brain abnormalities, inherited in an autosomal dominant pattern. This gene is highly intolerant to loss-of-function variants (pLI = 0.98), reflecting its critical role in neurodevelopment.

Summary from RefSeq, OMIM, UniProt
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Primary Disease Associations & Inheritance

Neurodevelopmental disorder with or without autistic features and/or structural brain abnormalitiesMIM #618859
AD
0
Active trials
9
Pubs (1 yr)
25
P/LP submissions
0%
P/LP missense
0.24
LOEUF· LoF intol.
LOF
Mechanism· predicted
Clinical SummaryNOVA2
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Gene-Disease Validity (ClinGen)
complex neurodevelopmental disorder · 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 0.98). One damaged copy is likely sufficient to cause disease.
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ClinVar Variants
23 unique Pathogenic / Likely Pathogenic· 74 VUS of 132 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Dual constrained — LoF & missense intolerant
LoF Constraint
0.24LOEUF
pLI 0.983
Z-score 3.25
OE 0.00 (0.000.24)
Highly constrained

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

Missense Constraint
4.35Z-score
OE missense 0.26 (0.210.31)
70 obs / 271.8 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.00 (0.000.24)
00.351.4
Missense OE0.26 (0.210.31)
00.61.4
Synonymous OE0.69
01.21.6
LoF obs/exp: 0 / 12.3Missense obs/exp: 70 / 271.8Syn Z: 2.88
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
strongNOVA2-related neurodevelopmental disorderOTHERAD
DN
0.3494th %ile
GOF
0.4085th %ile
LOF
0.83top 5%

The highest-scoring mechanism for this gene is loss-of-function (haploinsufficiency).

LOFprediction above median · 57% of P/LP variants are LoF · LOEUF 0.24

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

132 submitted variants in ClinVar

Classification Summary

Pathogenic17
Likely Pathogenic6
VUS74
Likely Benign24
Benign3
Conflicting3
17
Pathogenic
6
Likely Pathogenic
74
VUS
24
Likely Benign
3
Benign
3
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
10
0
7
0
17
Likely Pathogenic
3
0
3
0
6
VUS
3
55
15
1
74
Likely Benign
0
2
3
19
24
Benign
0
0
1
2
3
Conflicting
3
Total16572922127

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

View in ClinVar →

Protein Context — Lollipop Plot

NOVA2 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

Search ClinicalTrials.gov →
Clinical Literature
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