SMCO3

Chr 12

single-pass membrane protein with coiled-coil domains 3

Also known as: C12orf69

The SMCO3 protein is predicted to be located in cellular membranes, though its specific function remains unclear. Mutations in SMCO3 have been associated with neurodevelopmental disorders, though the clinical phenotype and inheritance pattern are not well-established from current data. This gene appears to tolerate loss-of-function variants well based on population genetic data.

Summary from RefSeq
Research Assistant →
0
Active trials
0
Pubs (1 yr)
40
P/LP submissions
0%
P/LP missense
1.63
LOEUF
Multiple*
Mechanism· predicted
Clinical SummarySMCO3
Population Constraint (gnomAD)
Low constraint (pLI 0.01) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
40 unique Pathogenic / Likely Pathogenic· 45 VUS of 87 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.63LOEUF
pLI 0.014
Z-score 0.62
OE 0.68 (0.311.63)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.17Z-score
OE missense 1.04 (0.901.21)
125 obs / 119.9 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.68 (0.311.63)
00.351.4
Missense OE1.04 (0.901.21)
00.61.4
Synonymous OE0.90
01.21.6
LoF obs/exp: 3 / 4.4Missense obs/exp: 125 / 119.9Syn Z: 0.50
DN
0.74top 25%
GOF
0.80top 10%
LOF
0.2287th %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

87 submitted variants in ClinVar

Classification Summary

Pathogenic38
Likely Pathogenic2
VUS45
Likely Benign1
38
Pathogenic
2
Likely Pathogenic
45
VUS
1
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
38
0
38
Likely Pathogenic
0
0
2
0
2
VUS
0
42
3
0
45
Likely Benign
0
1
0
0
1
Benign
0
0
0
0
0
Total04343086

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

View in ClinVar →

Protein Context — Lollipop Plot

SMCO3 · 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 2 results · since 2015Search PubMed ↗
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC