TMEM63B

Chr 6AD

transmembrane protein 63B

Also known as: C6orf110, DEE118, hTMEM63B

The TMEM63B protein functions as a mechanosensitive and osmosensitive cation channel that is essential for respiratory function, hearing, and cellular volume regulation, and also acts as a phospholipid scramblase in response to membrane structural changes. Mutations cause developmental and epileptic encephalopathy 118 with autosomal dominant inheritance. The gene is highly constrained against loss-of-function variants (pLI 1.0, LOEUF 0.168), reflecting its critical role in early development and essential physiological processes.

OMIMResearchSummary from RefSeq, OMIM, UniProt
GOFmechanismADLOEUF 0.171 OMIM phenotype
Clinical SummaryTMEM63B
Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 1.00). One damaged copy is likely sufficient to cause disease.
📋
ClinVar Variants
16 unique Pathogenic / Likely Pathogenic· 93 VUS of 161 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Dual constrained — LoF & missense intolerant
LoF Constraint
0.17LOEUF
pLI 1.000
Z-score 5.88
OE 0.07 (0.030.17)
Highly constrained

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

Missense Constraint
4.22Z-score
OE missense 0.48 (0.430.53)
243 obs / 511.4 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.07 (0.030.17)
00.351.4
Missense OE0.48 (0.430.53)
00.61.4
Synonymous OE1.10
01.21.6
LoF obs/exp: 3 / 46.1Missense obs/exp: 243 / 511.4Syn Z: -1.14
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
moderateTMEM63B-related developmental and epileptic encephalopathy with anemiaGOFAD
DN
0.4289th %ile
GOF
0.6932th %ile
LOF
0.53top 25%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and gain-of-function). The Badonyi & Marsh model scores gain-of-function highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports loss-of-function (haploinsufficiency). Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

LOFLOEUF 0.17
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. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

161 submitted variants in ClinVar

Classification Summary

Pathogenic12
Likely Pathogenic4
VUS93
Likely Benign14
Benign1
Conflicting1
12
Pathogenic
4
Likely Pathogenic
93
VUS
14
Likely Benign
1
Benign
1
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
4
8
0
12
Likely Pathogenic
0
3
1
0
4
VUS
5
86
2
0
93
Likely Benign
0
4
2
8
14
Benign
0
0
0
1
1
Conflicting
1
Total597139125

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

View in ClinVar →

Protein Context — Lollipop Plot

TMEM63B · 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
Open Research Assistant →
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC