COPS9

Chr 2

COP9 signalosome subunit 9

Also known as: CSNAP, MYEOV2

The COPS9 protein is a component of the COP9 signalosome complex that regulates protein degradation pathways by controlling the activity of cullin-RING E3 ubiquitin ligase complexes through deneddylation. Pathogenic variants in COPS9 cause autosomal recessive developmental and epileptic encephalopathy with microcephaly, characterized by early-onset seizures, severe developmental delay, and progressive microcephaly. This gene shows tolerance to loss-of-function variation (pLI 0.001), suggesting the disease mechanism may involve specific damaging variants rather than simple protein loss.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
1
Pubs (1 yr)
100
P/LP submissions
P/LP missense
1.48
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryCOPS9
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
98 unique Pathogenic / Likely Pathogenic· 9 VUS of 113 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.48LOEUF
pLI 0.001
Z-score 0.69
OE 0.72 (0.371.48)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.26Z-score
OE missense 1.06 (0.931.21)
154 obs / 145.1 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.72 (0.371.48)
00.351.4
Missense OE1.06 (0.931.21)
00.61.4
Synonymous OE1.08
01.21.6
LoF obs/exp: 5 / 7.0Missense obs/exp: 154 / 145.1Syn Z: -0.48
DN
0.7326th %ile
GOF
0.7029th %ile
LOF
0.3843th %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

113 submitted variants in ClinVar

Classification Summary

Pathogenic92
Likely Pathogenic6
VUS9
92
Pathogenic
6
Likely Pathogenic
9
VUS

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories· variant type breakdown unavailable

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
92
Likely Pathogenic
6
VUS
9
Likely Benign
0
Benign
0
Total107

Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

COPS9 · 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 ↗
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC

No open access results found