TBC1D14

Chr 4

TBC1 domain family member 14

The TBC1D14 protein regulates autophagosome formation during cellular starvation and controls trafficking of ATG9 from recycling endosomes to the Golgi apparatus to maintain the autophagy initiation machinery. Mutations cause autosomal recessive developmental and epileptic encephalopathy with movement abnormalities, typically presenting in infancy. The gene is highly constrained against loss-of-function variants (LOEUF 0.457), indicating intolerance to protein-disrupting mutations.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
2
Pubs (1 yr)
85
P/LP submissions
0%
P/LP missense
0.46
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryTBC1D14
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.27) despite low pLI — interpret in context.
📋
ClinVar Variants
85 unique Pathogenic / Likely Pathogenic· 91 VUS of 206 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.46LOEUF
pLI 0.039
Z-score 4.12
OE 0.27 (0.170.46)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
1.17Z-score
OE missense 0.84 (0.770.92)
346 obs / 412.7 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.27 (0.170.46)
00.351.4
Missense OE0.84 (0.770.92)
00.61.4
Synonymous OE1.11
01.21.6
LoF obs/exp: 10 / 37.1Missense obs/exp: 346 / 412.7Syn Z: -1.11
DN
0.76top 25%
GOF
0.74top 25%
LOF
0.3164th %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

206 submitted variants in ClinVar

Classification Summary

Pathogenic81
Likely Pathogenic4
VUS91
Likely Benign4
Benign2
81
Pathogenic
4
Likely Pathogenic
91
VUS
4
Likely Benign
2
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
81
0
81
Likely Pathogenic
0
0
4
0
4
VUS
0
88
3
0
91
Likely Benign
0
4
0
0
4
Benign
0
1
0
1
2
Total093881182

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

View in ClinVar →

Protein Context — Lollipop Plot

TBC1D14 · 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
Open Research Assistant →
Key Publications
Landmark & review papers · by relevance
PubMed
Top 1 results · since 2015Search PubMed ↗