SLC34A1

Chr 5ARAD

solute carrier family 34 member 1

Also known as: FRTS2, HCINF2, NAPI-3, NPHLOP1, NPT2, NPTIIa, SLC11, SLC17A2

The SLC34A1 protein is a sodium-phosphate cotransporter that actively transports phosphate into renal tubular cells with a 3:1 Na+:phosphate stoichiometry. Mutations cause autosomal recessive Fanconi renotubular syndrome, autosomal dominant infantile hypercalcemia, and hypophosphatemic nephrolithiasis with osteoporosis, affecting phosphate homeostasis and kidney function. The gene shows low constraint against loss-of-function variants (high LOEUF of 1.828), consistent with its association with both recessive and dominant inheritance patterns.

Summary from RefSeq, OMIM, UniProt
Research Assistant →

Primary Disease Associations & Inheritance

?Fanconi renotubular syndrome 2MIM #613388
AR
Hypercalcemia, infantile, 2MIM #616963
AR
Nephrolithiasis/osteoporosis, hypophosphatemic, 1MIM #612286
AD
0
Active trials
29
Pubs (1 yr)
73
P/LP submissions
6%
P/LP missense
1.83
LOEUF
Multiple*
Mechanism· predicted
Clinical SummarySLC34A1
🧬
Gene-Disease Validity (ClinGen)
hypercalcemia, infantile, 2 · ARDefinitive

Definitive — sufficient evidence for diagnostic panels

2 total gene-disease associations curated

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
63 unique Pathogenic / Likely Pathogenic· 251 VUS of 500 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.83LOEUF
pLI 0.000
Z-score -1.85
OE 1.41 (1.071.83)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.48Z-score
OE missense 1.07 (0.981.16)
400 obs / 374.1 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE1.41 (1.071.83)
00.351.4
Missense OE1.07 (0.981.16)
00.61.4
Synonymous OE1.02
01.21.6
LoF obs/exp: 34 / 24.2Missense obs/exp: 400 / 374.1Syn Z: -0.24
DN
0.76top 25%
GOF
0.73top 25%
LOF
0.3746th %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 · 1 literature citation
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.

Literature Evidence

DNThese results indicate that the mutant proteins altered the function of the wild-type NPT2a through a dominant negative effect.PMID:12324554

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

500 submitted variants in ClinVar

Classification Summary

Pathogenic34
Likely Pathogenic29
VUS251
Likely Benign150
Benign13
Conflicting20
34
Pathogenic
29
Likely Pathogenic
251
VUS
150
Likely Benign
13
Benign
20
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
12
0
22
0
34
Likely Pathogenic
18
4
7
0
29
VUS
7
219
23
2
251
Likely Benign
0
3
60
87
150
Benign
0
0
12
1
13
Conflicting
20
Total3722612490497

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

View in ClinVar →

Protein Context — Lollipop Plot

SLC34A1 · 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 →
Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
PubTator3
Top 5 full-text resultsSearch PubTator3 ↗