RAB11A

Chr 15

RAB11A, member RAS oncogene family

Also known as: YL8

The protein is a small GTPase that regulates both constitutive and regulated secretory pathways and protein transport at the cell membrane. Mutations cause autosomal dominant neurodevelopmental disorder with intellectual disability, seizures, and brain malformations through loss of function mechanisms. The high pLI score (0.99) and low LOEUF score (0.21) indicate the gene is highly intolerant to loss-of-function variants.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
45
Pubs (1 yr)
13
P/LP submissions
17%
P/LP missense
0.21
LOEUF· LoF intol.
Multiple*
Mechanism· predicted
Clinical SummaryRAB11A
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Gene-Disease Validity (ClinGen)
complex neurodevelopmental disorder with motor features · ADModerate

Moderate evidence — consider for supplementary testing

Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 0.99). One damaged copy is likely sufficient to cause disease.
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ClinVar Variants
12 unique Pathogenic / Likely Pathogenic· 51 VUS of 141 total submissions
Some data sources returned errors (1)

pubtator: TimeoutError: The operation was aborted due to timeout

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Dual constrained — LoF & missense intolerant
LoF Constraint
0.21LOEUF
pLI 0.992
Z-score 3.50
OE 0.00 (0.000.21)
Highly constrained

Highly LoF-intolerant (top ~10% of genes)

Missense Constraint
3.09Z-score
OE missense 0.22 (0.160.30)
27 obs / 123.8 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.00 (0.000.21)
00.351.4
Missense OE0.22 (0.160.30)
00.61.4
Synonymous OE1.07
01.21.6
LoF obs/exp: 0 / 14.3Missense obs/exp: 27 / 123.8Syn Z: -0.36
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
strongRAB11A-related epilepsy and intellectual disabilityOTHERAD
DN
0.6162th %ile
GOF
0.5759th %ile
LOF
0.64top 25%

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

LOFLOEUF 0.21
DNprediction 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. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

141 submitted variants in ClinVar

Classification Summary

Pathogenic8
Likely Pathogenic4
VUS51
Likely Benign58
Benign8
Conflicting3
8
Pathogenic
4
Likely Pathogenic
51
VUS
58
Likely Benign
8
Benign
3
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
8
0
8
Likely Pathogenic
0
2
2
0
4
VUS
0
42
8
1
51
Likely Benign
0
5
21
32
58
Benign
0
1
3
4
8
Conflicting
3
Total0504237132

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

View in ClinVar →

Protein Context — Lollipop Plot

RAB11A · 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 →
Clinical Literature
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