SLC30A8

Chr 8AD

solute carrier family 30 member 8

Also known as: ZNT8, ZnT-8

The protein encoded by this gene is a zinc efflux transporter involved in the accumulation of zinc in intracellular vesicles. This gene is expressed at a high level only in the pancreas, particularly in islets of Langerhans. The encoded protein colocalizes with insulin in the secretory pathway granules of the insulin-secreting INS-1 cells. Allelic variants of this gene exist that confer susceptibility to diabetes mellitus, noninsulin-dependent (NIDDM). Several transcript variants encoding different isoforms have been found for this gene.[provided by RefSeq, Mar 2010]

Primary Disease Associations & Inheritance

{Diabetes mellitus, noninsulin-dependent, susceptibility to}MIM #125853
AD
0
Active trials
15
Pubs (1 yr)
56
P/LP submissions
0%
P/LP missense
1.51
LOEUF
Multiple*
Mechanism· predicted
Clinical SummarySLC30A8
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
56 unique Pathogenic / Likely Pathogenic· 61 VUS of 134 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.51LOEUF
pLI 0.000
Z-score -0.05
OE 1.01 (0.691.51)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.11Z-score
OE missense 0.98 (0.871.10)
200 obs / 204.4 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE1.01 (0.691.51)
00.351.4
Missense OE0.98 (0.871.10)
00.61.4
Synonymous OE0.87
01.21.6
LoF obs/exp: 17 / 16.8Missense obs/exp: 200 / 204.4Syn Z: 0.91
DN
0.81top 10%
GOF
0.73top 25%
LOF
0.2583th %ile

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function and dominant-negative). The Badonyi & Marsh model scores dominant-negative highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports gain-of-function. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

GOFprediction above median · 1 literature citation
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.

Literature Evidence

GOFHere, we clarify this incongruence, showing that rs13266634 boosts the activity of an overlapping enhancer and suggesting an SLC30A8 gain of function as the cause for the increased risk for the disease.PMID:32912862

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

ClinVar Variant Classifications

134 submitted variants in ClinVar

Classification Summary

Pathogenic56
VUS61
Likely Benign7
Benign3
Conflicting1
56
Pathogenic
61
VUS
7
Likely Benign
3
Benign
1
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
56
0
56
Likely Pathogenic
0
0
0
0
0
VUS
2
50
9
0
61
Likely Benign
0
3
0
4
7
Benign
0
2
0
1
3
Conflicting
1
Total255655128

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

View in ClinVar →

Protein Context — Lollipop Plot

SLC30A8 · 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
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