RNF223

Chr 1

ring finger protein 223

The protein is predicted to function as an ubiquitin protein ligase that adds ubiquitin tags to proteins for degradation or regulation and localizes to cellular membranes. RNF223 mutations cause autosomal recessive developmental and epileptic encephalopathy with onset in infancy, characterized by severe intellectual disability, refractory seizures, and progressive brain atrophy. The gene shows tolerance to loss-of-function variants in the general population.

Summary from RefSeq
Research Assistant →
0
Active trials
1
Pubs (1 yr)
133
P/LP submissions
0%
P/LP missense
1.87
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryRNF223
Population Constraint (gnomAD)
Low constraint (pLI 0.03) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
126 unique Pathogenic / Likely Pathogenic· 92 VUS of 229 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.87LOEUF
pLI 0.027
Z-score 0.06
OE 0.95 (0.351.87)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.55Z-score
OE missense 1.15 (0.991.33)
124 obs / 107.8 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.95 (0.351.87)
00.351.4
Missense OE1.15 (0.991.33)
00.61.4
Synonymous OE1.15
01.21.6
LoF obs/exp: 2 / 2.1Missense obs/exp: 124 / 107.8Syn Z: -0.81
DN
0.6258th %ile
GOF
0.7127th %ile
LOF
0.4136th %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

229 submitted variants in ClinVar

Classification Summary

Pathogenic121
Likely Pathogenic5
VUS92
Likely Benign6
Benign5
121
Pathogenic
5
Likely Pathogenic
92
VUS
6
Likely Benign
5
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
121
0
121
Likely Pathogenic
0
0
5
0
5
VUS
0
70
22
0
92
Likely Benign
0
4
2
0
6
Benign
0
0
5
0
5
Total0741550229

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

View in ClinVar →

Protein Context — Lollipop Plot

RNF223 · 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.

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Clinical Literature
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