HERC2

Chr 15AR

HECT and RLD domain containing E3 ubiquitin protein ligase 2

Also known as: D15F37S1, MRT38, SHEP1, jdf2, p528

This gene encodes an E3 ubiquitin-protein ligase that regulates DNA damage repair by controlling ubiquitin-dependent retention of repair proteins on damaged chromosomes and modulates iron metabolism and insulin-like growth factor receptor signaling. Biallelic mutations cause autosomal recessive intellectual developmental disorder with onset typically in early childhood. The gene is highly constrained against loss-of-function variants in the general population, indicating that such variants are likely to be pathogenic when present in the homozygous or compound heterozygous state.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
LOFmechanismARLOEUF 0.203 OMIM phenotypes
Clinical SummaryHERC2
Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 1.00). One damaged copy is likely sufficient to cause disease.
📋
ClinVar Variants
12 unique Pathogenic / Likely Pathogenic· 327 VUS of 500 total submissions
📖
GeneReview available — HERC2
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Dual constrained — LoF & missense intolerant
LoF Constraint
0.20LOEUF
pLI 1.000
Z-score 12.07
OE 0.15 (0.120.20)
Highly constrained

Highly LoF-intolerant (top ~10% of genes)

Missense Constraint
4.42Z-score
OE missense 0.76 (0.730.79)
2105 obs / 2758.9 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.15 (0.120.20)
00.351.4
Missense OE0.76 (0.730.79)
00.61.4
Synonymous OE1.09
01.21.6
LoF obs/exp: 36 / 236.3Missense obs/exp: 2105 / 2758.9Syn Z: -2.51
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
strongHERC2-related neurodevelopmental disorderLOFAR

Predictions shown for reference only — model trained on dominant genes, not applicable to AR conditions.

DN
0.3395th %ile
GOF
0.2696th %ile
LOF
0.75top 10%

The Badonyi & Marsh prediction model was trained exclusively on dominant disease genes. Predictions are not reliable for genes with autosomal recessive inheritance and are shown at reduced opacity for reference only.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

500 submitted variants in ClinVar

Classification Summary

Pathogenic7
Likely Pathogenic5
VUS327
Likely Benign52
Conflicting1
7
Pathogenic
5
Likely Pathogenic
327
VUS
52
Likely Benign
1
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
1
0
6
0
7
Likely Pathogenic
3
1
1
0
5
VUS
0
314
11
2
327
Likely Benign
0
7
3
42
52
Benign
0
0
0
0
0
Conflicting
1
Total43222144392

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

View in ClinVar →

Protein Context — Lollipop Plot

HERC2 · protein map & ClinVar variants

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

3D Protein StructureAlphaFold

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

Search ClinicalTrials.gov →
Clinical Literature
Open Research Assistant →