NSG1

Chr 4

neuronal vesicle trafficking associated 1

Also known as: D4S234, D4S234E, NEEP21, P21

The NSG1 protein regulates neuronal receptor recycling, particularly AMPA receptors and L1CAM, which is critical for synaptic transmission and plasticity, and also has a role in apoptosis following DNA damage. Mutations cause neurodevelopmental disorders with intellectual disability, though the gene shows relatively low constraint to loss-of-function variants. The inheritance pattern has not been definitively established for NSG1-related disorders.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
3
Pubs (1 yr)
102
P/LP submissions
P/LP missense
1.29
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryNSG1
Population Constraint (gnomAD)
Low constraint (pLI 0.01) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
102 unique Pathogenic / Likely Pathogenic· 7 VUS of 111 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.29LOEUF
pLI 0.009
Z-score 1.07
OE 0.56 (0.281.29)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.37Z-score
OE missense 1.10 (0.951.27)
131 obs / 119.6 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.56 (0.281.29)
00.351.4
Missense OE1.10 (0.951.27)
00.61.4
Synonymous OE0.99
01.21.6
LoF obs/exp: 4 / 7.1Missense obs/exp: 131 / 119.6Syn Z: 0.06
DN
0.6260th %ile
GOF
0.6344th %ile
LOF
0.3648th %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

111 submitted variants in ClinVar

Classification Summary

Pathogenic98
Likely Pathogenic4
VUS7
Likely Benign1
98
Pathogenic
4
Likely Pathogenic
7
VUS
1
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories· variant type breakdown unavailable

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
98
Likely Pathogenic
4
VUS
7
Likely Benign
1
Benign
0
Total110

Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

NSG1 · 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.

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Clinical Literature
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