AP1S3

Chr 2AD

adaptor related protein complex 1 subunit sigma 3

Also known as: PSORS15, sigma1C

The AP1S3 protein is a subunit of clathrin-associated adaptor protein complex 1 that mediates protein sorting in the late-Golgi/trans-Golgi network and endosomes, including trafficking of TLR3. Mutations cause autosomal dominant pustular psoriasis (psoriasis 15), which primarily affects the skin rather than the nervous system. This gene shows low constraint to loss-of-function variants (pLI 0.016, LOEUF 1.079), suggesting it may not be associated with severe developmental disorders.

Summary from RefSeq, OMIM, UniProt
Research Assistant →

Primary Disease Associations & Inheritance

{Psoriasis 15, pustular, susceptibility to}MIM #616106
AD
1
Active trials
5
Pubs (1 yr)
31
P/LP submissions
0%
P/LP missense
1.08
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryAP1S3
Population Constraint (gnomAD)
Low constraint (pLI 0.02) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
31 unique Pathogenic / Likely Pathogenic· 17 VUS of 78 total submissions
💊
Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.08LOEUF
pLI 0.016
Z-score 1.43
OE 0.47 (0.231.08)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.51Z-score
OE missense 0.84 (0.691.03)
70 obs / 83.0 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.47 (0.231.08)
00.351.4
Missense OE0.84 (0.691.03)
00.61.4
Synonymous OE0.68
01.21.6
LoF obs/exp: 4 / 8.5Missense obs/exp: 70 / 83.0Syn Z: 1.31
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
strongAP1S3-related psoriasis, pustular, susceptibility toOTHERAD
DN
0.75top 25%
GOF
0.6834th %ile
LOF
0.2385th %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

78 submitted variants in ClinVar

Classification Summary

Pathogenic30
Likely Pathogenic1
VUS17
Likely Benign14
Benign9
30
Pathogenic
1
Likely Pathogenic
17
VUS
14
Likely Benign
9
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
30
0
30
Likely Pathogenic
0
0
1
0
1
VUS
0
12
5
0
17
Likely Benign
0
5
7
2
14
Benign
0
1
8
0
9
Total01851271

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

View in ClinVar →

Protein Context — Lollipop Plot

AP1S3 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

Clinical Literature
Open Research Assistant →
Key Publications
Landmark & review papers · by relevance
PubMed
Top 5 results · since 2015Search PubMed ↗