RAB17

Chr 2

RAB17, member RAS oncogene family

RAB17 encodes an epithelial cell-specific small GTPase that regulates intracellular membrane trafficking, particularly controlling transcytosis (the directed movement of materials through cells) and melanosome transport, and is required for dendrite and dendritic spine development. Mutations in RAB17 cause autosomal recessive infantile-onset symptomatic epilepsy syndrome, which presents in early infancy with seizures and developmental delays. The gene shows low constraint to loss-of-function variants, consistent with its recessive inheritance pattern.

Summary from RefSeq, UniProt
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0
Active trials
6
Pubs (1 yr)
79
P/LP submissions
0%
P/LP missense
0.95
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryRAB17
Population Constraint (gnomAD)
Low constraint (pLI 0.07) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
77 unique Pathogenic / Likely Pathogenic· 47 VUS of 135 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.95LOEUF
pLI 0.075
Z-score 1.68
OE 0.37 (0.170.95)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.07Z-score
OE missense 0.98 (0.851.14)
124 obs / 126.2 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.37 (0.170.95)
00.351.4
Missense OE0.98 (0.851.14)
00.61.4
Synonymous OE0.97
01.21.6
LoF obs/exp: 3 / 8.2Missense obs/exp: 124 / 126.2Syn Z: 0.21
DN
0.85top 5%
GOF
0.76top 25%
LOF
0.1895th %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

135 submitted variants in ClinVar

Classification Summary

Pathogenic76
Likely Pathogenic1
VUS47
Likely Benign3
76
Pathogenic
1
Likely Pathogenic
47
VUS
3
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
76
0
76
Likely Pathogenic
0
0
1
0
1
VUS
0
35
12
0
47
Likely Benign
0
2
1
0
3
Benign
0
0
0
0
0
Total037900127

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

View in ClinVar →

Protein Context — Lollipop Plot

RAB17 · 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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