SLC19A1

Chr 21AR

solute carrier family 19 member 1

Also known as: CHMD, FOLT, IFC-1, IFC1, IMD114, MEGAF, REFC, RFC

The encoded protein is an antiporter that mediates cellular import of reduced folates, particularly N5-methyltetrahydrofolate, and also transports immunoreactive cyclic dinucleotides involved in immune signaling. Autosomal recessive mutations cause folate-responsive megaloblastic anemia and immunodeficiency 114, both responding to folate supplementation. The gene shows tolerance to loss-of-function variants (LOEUF 1.164), suggesting that complete loss of function from both alleles is required for disease manifestation.

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

?Megaloblastic anemia, folate-responsiveMIM #601775
AR
Immunodeficiency 114, folate-responsiveMIM #620603
AR
0
Active trials
21
Pubs (1 yr)
0
P/LP submissions
P/LP missense
1.16
LOEUF
Multiple*
Mechanism· predicted
Clinical SummarySLC19A1
🧬
Gene-Disease Validity (ClinGen)
immunodeficiency 114, folate-responsive · ARLimited

Limited evidence — not for standalone diagnostic reporting

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.16LOEUF
pLI 0.000
Z-score 1.11
OE 0.69 (0.421.16)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.61Z-score
OE missense 0.91 (0.841.00)
350 obs / 383.4 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.69 (0.421.16)
00.351.4
Missense OE0.91 (0.841.00)
00.61.4
Synonymous OE1.03
01.21.6
LoF obs/exp: 10 / 14.6Missense obs/exp: 350 / 383.4Syn Z: -0.28
DN
0.7228th %ile
GOF
0.74top 25%
LOF
0.3066th %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

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

SLC19A1 · 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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