SLC9A8

Chr 20

solute carrier family 9 member A8

Also known as: NHE-8, NHE8

SLC9A8 encodes a sodium-hydrogen antiporter that exchanges intracellular H+ for extracellular Na+ in 1:1 stoichiometry, functioning primarily in the trans-Golgi to regulate pH and protein trafficking, and also contributing to intestinal sodium absorption and retinal pigment epithelium pH homeostasis. Mutations cause autosomal recessive intellectual developmental disorder with seizures, microcephaly, and cerebellar atrophy. This gene is not constrained against loss-of-function variants, consistent with its recessive inheritance pattern.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
1
Pubs (1 yr)
9
P/LP submissions
0%
P/LP missense
1.01
LOEUF
Multiple*
Mechanism· predicted
Clinical SummarySLC9A8
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
9 unique Pathogenic / Likely Pathogenic· 60 VUS of 102 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.01LOEUF
pLI 0.000
Z-score 1.50
OE 0.69 (0.481.01)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
1.62Z-score
OE missense 0.76 (0.680.84)
266 obs / 351.4 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.69 (0.481.01)
00.351.4
Missense OE0.76 (0.680.84)
00.61.4
Synonymous OE1.07
01.21.6
LoF obs/exp: 19 / 27.5Missense obs/exp: 266 / 351.4Syn Z: -0.63
DN
0.83top 10%
GOF
0.79top 25%
LOF
0.2288th %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

102 submitted variants in ClinVar

Classification Summary

Pathogenic7
Likely Pathogenic2
VUS60
Likely Benign5
7
Pathogenic
2
Likely Pathogenic
60
VUS
5
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
7
0
7
Likely Pathogenic
0
0
2
0
2
VUS
0
57
3
0
60
Likely Benign
0
2
0
3
5
Benign
0
0
0
0
0
Total05912374

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

View in ClinVar →

Protein Context — Lollipop Plot

SLC9A8 · 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 →