TBC1D5

Chr 3

TBC1 domain family member 5

TBC1D5 encodes a GTPase-activating protein that regulates retrograde transport from endosomes to the Golgi and controls autophagy by modulating vesicle trafficking. Biallelic mutations cause early-onset neurodevelopmental disorder with intellectual disability, seizures, and movement abnormalities, following autosomal recessive inheritance. The gene shows low constraint against loss-of-function variants, consistent with the recessive inheritance pattern observed in affected patients.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 0.97
Clinical SummaryTBC1D5
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
24 unique Pathogenic / Likely Pathogenic· 104 VUS of 162 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.97LOEUF
pLI 0.000
Z-score 1.74
OE 0.73 (0.550.97)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.69Z-score
OE missense 0.91 (0.830.99)
383 obs / 422.7 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.73 (0.550.97)
00.351.4
Missense OE0.91 (0.830.99)
00.61.4
Synonymous OE1.03
01.21.6
LoF obs/exp: 34 / 46.9Missense obs/exp: 383 / 422.7Syn Z: -0.30
DN
0.6840th %ile
GOF
0.6736th %ile
LOF
0.4233th %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

162 submitted variants in ClinVar

Classification Summary

Pathogenic23
Likely Pathogenic1
VUS104
Likely Benign9
23
Pathogenic
1
Likely Pathogenic
104
VUS
9
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
23
0
23
Likely Pathogenic
0
0
1
0
1
VUS
0
97
7
0
104
Likely Benign
1
6
2
0
9
Benign
0
0
0
0
0
Total1103330137

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

View in ClinVar →

Protein Context — Lollipop Plot

TBC1D5 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold

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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