ASB5

Chr 4

ankyrin repeat and SOCS box containing 5

Also known as: ASB-5

The ASB5 protein functions as a substrate-recognition component of an E3 ubiquitin ligase complex that targets proteins for degradation and may play a role in blood vessel development. Mutations cause autosomal recessive developmental and epileptic encephalopathy with onset in infancy or early childhood, characterized by seizures, developmental delay, and neurological regression. The gene shows minimal constraint against loss-of-function variants, consistent with its recessive inheritance pattern.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
2
Pubs (1 yr)
76
P/LP submissions
0%
P/LP missense
1.50
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryASB5
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
76 unique Pathogenic / Likely Pathogenic· 57 VUS of 139 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.50LOEUF
pLI 0.000
Z-score -0.09
OE 1.02 (0.711.50)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.22Z-score
OE missense 1.05 (0.931.18)
192 obs / 183.6 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE1.02 (0.711.50)
00.351.4
Missense OE1.05 (0.931.18)
00.61.4
Synonymous OE0.95
01.21.6
LoF obs/exp: 19 / 18.6Missense obs/exp: 192 / 183.6Syn Z: 0.32
DN
0.6745th %ile
GOF
0.6931th %ile
LOF
0.3162th %ile

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function and dominant-negative). Both the Badonyi & Marsh prediction and the broader genomic evidence point to gain-of-function as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

GOFprediction above median
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.

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

ClinVar Variant Classifications

139 submitted variants in ClinVar

Classification Summary

Pathogenic74
Likely Pathogenic2
VUS57
Likely Benign1
74
Pathogenic
2
Likely Pathogenic
57
VUS
1
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
74
0
74
Likely Pathogenic
0
0
2
0
2
VUS
0
52
5
0
57
Likely Benign
0
1
0
0
1
Benign
0
0
0
0
0
Total053810134

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

View in ClinVar →

Protein Context — Lollipop Plot

ASB5 · 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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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