SLC16A11

Chr 17

solute carrier family 16 member 11

Also known as: MCT 11, MCT11

The protein functions as a proton-linked monocarboxylate transporter that catalyzes pyruvate transport across the plasma membrane and is involved in hepatic lipid metabolism. Based on the extremely low pLI score and high LOEUF value, this gene appears highly tolerant to loss-of-function variants, with predicted gain-of-function being the likely pathogenic mechanism. However, no specific pediatric neurologic diseases have been definitively associated with SLC16A11 mutations in the provided data.

Summary from RefSeq, UniProt, Mechanism
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Primary Disease Associations & Inheritance

UniProtType 2 diabetes mellitus
1
Active trials
4
Pubs (1 yr)
19
P/LP submissions
0%
P/LP missense
1.44
LOEUF
Multiple*
Mechanism· predicted
Clinical SummarySLC16A11
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
19 unique Pathogenic / Likely Pathogenic· 97 VUS of 122 total submissions
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Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available
Some data sources returned errors (1)

ensembl: TimeoutError: The operation was aborted due to timeout

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.44LOEUF
pLI 0.000
Z-score 0.51
OE 0.83 (0.501.44)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.38Z-score
OE missense 0.93 (0.841.04)
244 obs / 261.2 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.83 (0.501.44)
00.351.4
Missense OE0.93 (0.841.04)
00.61.4
Synonymous OE1.00
01.21.6
LoF obs/exp: 9 / 10.8Missense obs/exp: 244 / 261.2Syn Z: -0.01
DN
0.74top 25%
GOF
0.85top 5%
LOF
0.2385th %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

122 submitted variants in ClinVar

Classification Summary

Pathogenic18
Likely Pathogenic1
VUS97
Likely Benign4
Benign1
18
Pathogenic
1
Likely Pathogenic
97
VUS
4
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
18
0
18
Likely Pathogenic
0
0
1
0
1
VUS
0
85
12
0
97
Likely Benign
0
4
0
0
4
Benign
0
1
0
0
1
Total090310121

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

View in ClinVar →

Protein Context — Lollipop Plot

SLC16A11 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

Clinical Literature
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Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC