SLC26A7

Chr 8

solute carrier family 26 member 7

Also known as: SUT2

This gene is one member of a family of sulfate/anion transporter genes. Family members are well conserved in gene structure and protein length yet have markedly different tissue expression patterns. This gene has abundant and specific expression in the kidney. Alternatively spliced transcript variants that encode different isoforms have been described. [provided by RefSeq, Aug 2013]

0
Active trials
8
Pubs (1 yr)
38
P/LP submissions
3%
P/LP missense
0.81
LOEUF
Multiple*
Mechanism· predicted
Clinical SummarySLC26A7
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
38 unique Pathogenic / Likely Pathogenic· 102 VUS of 162 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.81LOEUF
pLI 0.000
Z-score 2.48
OE 0.55 (0.390.81)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.01Z-score
OE missense 1.00 (0.911.09)
351 obs / 351.6 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.55 (0.390.81)
00.351.4
Missense OE1.00 (0.911.09)
00.61.4
Synonymous OE1.02
01.21.6
LoF obs/exp: 20 / 36.1Missense obs/exp: 351 / 351.6Syn Z: -0.15
DN
0.81top 10%
GOF
0.78top 25%
LOF
0.2091th %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

162 submitted variants in ClinVar

Classification Summary

Pathogenic35
Likely Pathogenic3
VUS102
Likely Benign5
Benign1
35
Pathogenic
3
Likely Pathogenic
102
VUS
5
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
1
0
34
0
35
Likely Pathogenic
1
1
1
0
3
VUS
0
96
6
0
102
Likely Benign
0
4
1
0
5
Benign
0
1
0
0
1
Total2102420146

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

View in ClinVar →

Protein Context — Lollipop Plot

SLC26A7 · 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 →
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC