ARGLU1

Chr 13

arginine and glutamate rich 1

This protein functions as a dual regulator of gene expression, serving as a transcriptional coactivator for nuclear receptors and directly modulating alternative splicing of pre-mRNAs through binding to spliceosome components. Mutations cause neurodevelopmental disorders affecting the central nervous system, heart development, and neuronal function. The gene shows autosomal dominant inheritance and is highly constrained against loss-of-function variants, indicating that even single functional copies are critical for normal development.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
3
Pubs (1 yr)
110
P/LP submissions
0%
P/LP missense
0.39
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryARGLU1
Population Constraint (gnomAD)
Moderately constrained gene (pLI 0.86) — some intolerance to loss-of-function variants.
📋
ClinVar Variants
110 unique Pathogenic / Likely Pathogenic· 21 VUS of 142 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.39LOEUF
pLI 0.862
Z-score 3.48
OE 0.15 (0.070.39)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
2.48Z-score
OE missense 0.44 (0.360.54)
70 obs / 157.6 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.15 (0.070.39)
00.351.4
Missense OE0.44 (0.360.54)
00.61.4
Synonymous OE1.13
01.21.6
LoF obs/exp: 3 / 19.7Missense obs/exp: 70 / 157.6Syn Z: -0.80
DN
0.6454th %ile
GOF
0.6638th %ile
LOF
0.62top 25%

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
LOFLOEUF 0.39

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

142 submitted variants in ClinVar

Classification Summary

Pathogenic109
Likely Pathogenic1
VUS21
Likely Benign3
Benign1
109
Pathogenic
1
Likely Pathogenic
21
VUS
3
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
109
0
109
Likely Pathogenic
0
0
1
0
1
VUS
0
14
7
0
21
Likely Benign
0
0
0
3
3
Benign
0
1
0
0
1
Total0151173135

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

View in ClinVar →

Protein Context — Lollipop Plot

ARGLU1 · 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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