ARHGAP22

Chr 10

Rho GTPase activating protein 22

Also known as: RhoGAP2, RhoGap22

The protein acts as a GTPase-activating protein that regulates RAC1 signaling and controls endothelial cell capillary tube formation during angiogenesis, while also inhibiting lamellipodia formation involved in cell motility. Mutations cause autosomal recessive intellectual disability with macrocephaly, seizures, and spasticity. The gene shows very low constraint against loss-of-function variants, consistent with a recessive inheritance pattern.

Summary from RefSeq, UniProt
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0
Active trials
3
Pubs (1 yr)
58
P/LP submissions
0%
P/LP missense
0.92
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryARHGAP22
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
58 unique Pathogenic / Likely Pathogenic· 164 VUS of 260 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.92LOEUF
pLI 0.000
Z-score 1.89
OE 0.62 (0.430.92)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.60Z-score
OE missense 0.92 (0.851.00)
413 obs / 448.6 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.62 (0.430.92)
00.351.4
Missense OE0.92 (0.851.00)
00.61.4
Synonymous OE0.96
01.21.6
LoF obs/exp: 18 / 29.0Missense obs/exp: 413 / 448.6Syn Z: 0.47
DN
0.7228th %ile
GOF
0.6638th %ile
LOF
0.3549th %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

260 submitted variants in ClinVar

Classification Summary

Pathogenic37
Likely Pathogenic21
VUS164
Likely Benign11
Benign4
37
Pathogenic
21
Likely Pathogenic
164
VUS
11
Likely Benign
4
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
37
0
37
Likely Pathogenic
0
0
21
0
21
VUS
1
133
30
0
164
Likely Benign
0
7
3
1
11
Benign
0
1
1
2
4
Total1141923237

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

View in ClinVar →

Protein Context — Lollipop Plot

ARHGAP22 · 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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