TMBIM4

Chr 12

transmembrane BAX inhibitor motif containing 4

Also known as: CGI-119, GAAP, LFG4, S1R, ZPRO

The TMBIM4 protein functions as an anti-apoptotic protein that inhibits cell death and modulates calcium signaling through capacitative calcium entry and IP3-mediated calcium release from the endoplasmic reticulum and Golgi. Mutations in TMBIM4 cause autosomal recessive spinal muscular atrophy with congenital bone fractures, characterized by early-onset neuromuscular weakness and skeletal fragility. The gene shows tolerance to loss-of-function variants (LOEUF 1.487), suggesting that complete loss of protein function may be required for disease manifestation.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 1.49
Clinical SummaryTMBIM4
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
15 unique Pathogenic / Likely Pathogenic· 34 VUS of 65 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.49LOEUF
pLI 0.000
Z-score 0.43
OE 0.86 (0.521.49)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.51Z-score
OE missense 0.87 (0.731.02)
98 obs / 113.3 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.86 (0.521.49)
00.351.4
Missense OE0.87 (0.731.02)
00.61.4
Synonymous OE0.82
01.21.6
LoF obs/exp: 9 / 10.5Missense obs/exp: 98 / 113.3Syn Z: 0.96
DN
0.83top 10%
GOF
0.89top 5%
LOF
0.1399th %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

65 submitted variants in ClinVar

Classification Summary

Pathogenic15
VUS34
Likely Benign3
15
Pathogenic
34
VUS
3
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
15
0
15
Likely Pathogenic
0
0
0
0
0
VUS
2
28
4
0
34
Likely Benign
0
2
0
1
3
Benign
0
0
0
0
0
Total23019152

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

View in ClinVar →

Protein Context — Lollipop Plot

TMBIM4 · 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.

Search ClinicalTrials.gov →
Clinical Literature
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