ADAM7

Chr 8

ADAM metallopeptidase domain 7

Also known as: ADAM 7, ADAM-7, EAPI, GP-83, GP83

The protein is a non-catalytic member of the ADAM family of zinc proteases that is required for normal male fertility by maintaining epithelial cell morphology in the epididymis and playing a role in sperm motility and capacitation. Mutations in this gene may be involved in melanoma progression, though no established Mendelian pediatric neurological disorders are currently associated with ADAM7 variants. The gene shows no constraint against loss-of-function variants (very low pLI score), suggesting haploinsufficiency is unlikely to cause disease.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
5
Pubs (1 yr)
82
P/LP submissions
0%
P/LP missense
1.03
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryADAM7
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
82 unique Pathogenic / Likely Pathogenic· 131 VUS of 227 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.03LOEUF
pLI 0.000
Z-score 1.38
OE 0.78 (0.591.03)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.51Z-score
OE missense 1.07 (0.991.16)
427 obs / 398.6 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.78 (0.591.03)
00.351.4
Missense OE1.07 (0.991.16)
00.61.4
Synonymous OE1.02
01.21.6
LoF obs/exp: 35 / 45.0Missense obs/exp: 427 / 398.6Syn Z: -0.15
DN
0.6647th %ile
GOF
0.6639th %ile
LOF
0.2680th %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

227 submitted variants in ClinVar

Classification Summary

Pathogenic78
Likely Pathogenic4
VUS131
Likely Benign8
Benign1
78
Pathogenic
4
Likely Pathogenic
131
VUS
8
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
78
0
78
Likely Pathogenic
0
0
4
0
4
VUS
0
123
8
0
131
Likely Benign
0
6
0
2
8
Benign
0
0
1
0
1
Total0129912222

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

View in ClinVar →

Protein Context — Lollipop Plot

ADAM7 · 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 →
Key Publications
Landmark & review papers · by relevance
PubMed
Top 1 results · since 2015Search PubMed ↗