RASA3

Chr 13

RAS p21 protein activator 3

Also known as: GAP1IP4BP, GAPIII

The protein functions as a GTPase-activating protein that negatively regulates Ras signaling by stimulating the GTPase activity of Ras p21 and binds inositol tetrakisphosphate with high affinity. Mutations in this gene cause microcephaly, seizures, intellectual disability, and cataracts, typically presenting in infancy with autosomal recessive inheritance. The gene is not highly constrained against loss-of-function variants, which is consistent with the recessive inheritance pattern observed clinically.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
6
Pubs (1 yr)
119
P/LP submissions
1%
P/LP missense
0.71
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryRASA3
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
119 unique Pathogenic / Likely Pathogenic· 143 VUS of 311 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.71LOEUF
pLI 0.000
Z-score 3.16
OE 0.50 (0.360.71)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
1.68Z-score
OE missense 0.79 (0.730.86)
416 obs / 524.3 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.50 (0.360.71)
00.351.4
Missense OE0.79 (0.730.86)
00.61.4
Synonymous OE1.17
01.21.6
LoF obs/exp: 24 / 47.5Missense obs/exp: 416 / 524.3Syn Z: -2.01
DN
0.7132th %ile
GOF
0.6735th %ile
LOF
0.3260th %ile

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative and gain-of-function). Both the Badonyi & Marsh prediction and the broader genomic evidence point to dominant-negative as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

DNprediction above median
GOFprediction 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

311 submitted variants in ClinVar

Classification Summary

Pathogenic115
Likely Pathogenic4
VUS143
Likely Benign13
Benign5
115
Pathogenic
4
Likely Pathogenic
143
VUS
13
Likely Benign
5
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
1
0
114
0
115
Likely Pathogenic
0
1
3
0
4
VUS
0
123
20
0
143
Likely Benign
0
4
4
5
13
Benign
0
0
2
3
5
Total11281438280

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

View in ClinVar →

Protein Context — Lollipop Plot

RASA3 · 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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