SLC47A1

Chr 17

solute carrier family 47 member 1

Also known as: MATE1

The protein functions as a multidrug efflux pump that transports cationic compounds including endogenous metabolites, drugs, and toxins through the kidney and liver for excretion in urine and bile. This gene shows extremely low constraint against loss-of-function variants (pLI ~0), and no clear disease associations have been established from mutations in SLC47A1. The gene is located within the Smith-Magenis syndrome region on chromosome 17, but deletions causing this syndrome typically involve multiple genes.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 1.17
Clinical SummarySLC47A1
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
80 unique Pathogenic / Likely Pathogenic· 14 VUS of 100 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.17LOEUF
pLI 0.000
Z-score 0.85
OE 0.83 (0.601.17)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.19Z-score
OE missense 1.03 (0.941.13)
334 obs / 324.6 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.83 (0.601.17)
00.351.4
Missense OE1.03 (0.941.13)
00.61.4
Synonymous OE1.04
01.21.6
LoF obs/exp: 24 / 28.9Missense obs/exp: 334 / 324.6Syn Z: -0.39
DN
0.6744th %ile
GOF
0.72top 25%
LOF
0.3067th %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

100 submitted variants in ClinVar

Classification Summary

Pathogenic78
Likely Pathogenic2
VUS14
Likely Benign3
Benign3
78
Pathogenic
2
Likely Pathogenic
14
VUS
3
Likely Benign
3
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories· variant type breakdown unavailable

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
78
Likely Pathogenic
2
VUS
14
Likely Benign
3
Benign
3
Total100

Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

SLC47A1 · 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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