RAB9B

Chr X

RAB9B, member RAS oncogene family

Also known as: RAB9L, Rab-9L

RAB9B encodes a small GTPase that regulates intracellular membrane trafficking, specifically controlling transport of proteins between endosomes and the trans-Golgi network by cycling between inactive GDP-bound and active GTP-bound forms. Mutations cause autosomal dominant neurological disease through a predicted gain-of-function mechanism. The protein uses NDE1/NDEL1 as an effector to interact with the dynein motor complex for retrograde trafficking of late endosomes to the trans-Golgi network.

Summary from RefSeq, UniProt, Mechanism
Research Assistant →
0
Active trials
2
Pubs (1 yr)
260
P/LP submissions
27%
P/LP missense
0.68
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryRAB9B
Population Constraint (gnomAD)
Moderately constrained gene (pLI 0.73) — some intolerance to loss-of-function variants.
📋
ClinVar Variants
212 unique Pathogenic / Likely Pathogenic· 89 VUS of 400 total submissions
Some data sources returned errors (1)

ensembl: TimeoutError: The operation was aborted due to timeout

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.68LOEUF
pLI 0.734
Z-score 1.94
OE 0.00 (0.000.68)
Moderately constrained

Typical tolerance to LoF variation

Missense Constraint
1.80Z-score
OE missense 0.42 (0.320.57)
33 obs / 77.8 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.00 (0.000.68)
00.351.4
Missense OE0.42 (0.320.57)
00.61.4
Synonymous OE1.15
01.21.6
LoF obs/exp: 0 / 4.4Missense obs/exp: 33 / 77.8Syn Z: -0.67
DN
0.6454th %ile
GOF
0.73top 25%
LOF
0.4038th %ile

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

GOFprediction above median
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.

ClinVar Variant Classifications

400 submitted variants in ClinVar

Classification Summary

Pathogenic127
Likely Pathogenic85
VUS89
Likely Benign69
Benign21
Conflicting8
127
Pathogenic
85
Likely Pathogenic
89
VUS
69
Likely Benign
21
Benign
8
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
19
8
100
0
127
Likely Pathogenic
19
50
13
3
85
VUS
0
68
19
2
89
Likely Benign
0
2
30
37
69
Benign
0
2
15
4
21
Conflicting
8
Total3813017746399

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

View in ClinVar →

Protein Context — Lollipop Plot

RAB9B · 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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