ARHGEF26

Chr 3

Rho guanine nucleotide exchange factor 26

Also known as: CSGEF, HMFN1864, SGEF

This gene encodes a member of the Rho-guanine nucleotide exchange factor (Rho-GEF) family. These proteins regulate Rho GTPases by catalyzing the exchange of GDP for GTP. The encoded protein specifically activates RhoG and plays a role in the promotion of macropinocytosis. Underexpression of the encoded protein may be a predictive marker of chemoresistant disease. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene. [provided by RefSeq, Oct 2011]

OMIMResearchGenerating clinical summary…
MultiplemechanismLOEUF 0.99
Clinical SummaryARHGEF26
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
1 unique Pathogenic / Likely Pathogenic· 135 VUS of 160 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint?
0.99LOEUF
pLI 0.000
Z-score 1.60
OE 0.72 (0.530.99)
Tolerant

Typical tolerance to LoF variation

Missense Constraint?
-1.02Z-score
OE missense 1.13 (1.051.22)
519 obs / 457.7 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios?
LoF OE?0.72 (0.530.99)
00.351.4
Missense OE?1.13 (1.051.22)
00.61.4
Synonymous OE?1.26
01.21.6
LoF obs/exp: 27 / 37.6Missense obs/exp: 519 / 457.7Syn Z: -2.80

This gene — mechanism propensity

DN
0.6453th %ile
GOF
0.6345th %ile
LOF
0.4529th %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

160 submitted variants in ClinVar

Classification Summary

Likely Pathogenic1
VUS135
Likely Benign4
1
Likely Pathogenic
135
VUS
4
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
0
0
0
Likely Pathogenic
1
0
0
0
1
VUS
0
135
0
0
135
Likely Benign
0
4
0
0
4
Benign
0
0
0
0
0
Total113900140

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

View in ClinVar →

16 pathogenic / likely-pathogenic (of 21) ClinVar copy-number / structural variants overlap ARHGEF26 — these span large chromosomal regions, not the gene specifically, and are excluded from the counts above. Explore in CNV tools →

Protein Context — Lollipop Plot

ARHGEF26 · 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 →