SLC25A39

Chr 17

solute carrier family 25 member 39

Also known as: CGI-69, CGI69

The protein functions as a mitochondrial transporter that imports glutathione from the cytosol into mitochondria, where it is essential for iron-sulfur cluster protein stability and erythropoiesis. Biallelic mutations cause a severe mitochondrial disorder characterized by early-onset developmental delay, hypotonia, seizures, and often early lethality, following an autosomal recessive inheritance pattern. The pathogenic mechanism involves loss of mitochondrial glutathione import, leading to oxidative stress and impaired iron-sulfur cluster metabolism.

Summary from RefSeq, UniProt, Mechanism
0
Active trials
16
Pubs (1 yr)
10
P/LP submissions
0%
P/LP missense
1.22
LOEUF
DN
Mechanism· predicted
Clinical SummarySLC25A39
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
10 unique Pathogenic / Likely Pathogenic· 82 VUS of 115 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.22LOEUF
pLI 0.000
Z-score 0.76
OE 0.82 (0.571.22)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.30Z-score
OE missense 0.94 (0.841.06)
212 obs / 224.5 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.82 (0.571.22)
00.351.4
Missense OE0.94 (0.841.06)
00.61.4
Synonymous OE1.42
01.21.6
LoF obs/exp: 18 / 21.8Missense obs/exp: 212 / 224.5Syn Z: -3.14
DN
0.78top 25%
GOF
0.72top 25%
LOF
0.3357th %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

115 submitted variants in ClinVar

Classification Summary

Pathogenic10
VUS82
Likely Benign5
10
Pathogenic
82
VUS
5
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
10
0
10
Likely Pathogenic
0
0
0
0
0
VUS
0
81
1
0
82
Likely Benign
0
4
0
1
5
Benign
0
0
0
0
0
Total08511197

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

View in ClinVar →

Protein Context — Lollipop Plot

SLC25A39 · 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.

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Clinical Literature
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