RNF213

Chr 17ADAR

ring finger protein 213

Also known as: ALO17, C17orf27, KIAA1618, MYMY2, MYSTR, NET57

The protein functions as an atypical E3 ubiquitin ligase with ATPase activity that catalyzes ubiquitination of both proteins and lipids, playing roles in lipid metabolism, angiogenesis, cell-autonomous immunity, and vascular development through the non-canonical Wnt signaling pathway. Mutations cause susceptibility to Moyamoya disease, a vascular disorder affecting intracranial arteries, with both autosomal dominant and autosomal recessive inheritance patterns reported. The pathogenic mechanism involves dominant-negative effects that likely disrupt the protein's critical ubiquitin ligase and ATPase functions.

Summary from RefSeq, OMIM, UniProt, Mechanism
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Primary Disease Associations & Inheritance

{Moyamoya disease 2, susceptibility to}MIM #607151
ADAR
0
Active trials
94
Pubs (1 yr)
28
P/LP submissions
52%
P/LP missense
0.66
LOEUF
DN
Mechanism· predicted
Clinical SummaryRNF213
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
27 unique Pathogenic / Likely Pathogenic· 345 VUS of 898 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.66LOEUF
pLI 0.000
Z-score 6.01
OE 0.57 (0.490.66)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
2.30Z-score
OE missense 0.88 (0.850.91)
2539 obs / 2887.0 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.57 (0.490.66)
00.351.4
Missense OE0.88 (0.850.91)
00.61.4
Synonymous OE1.07
01.21.6
LoF obs/exp: 126 / 222.8Missense obs/exp: 2539 / 2887.0Syn Z: -2.04
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
moderateRNF213-related moyamoya diseaseOTHERAD
DN
0.6744th %ile
GOF
0.4382th %ile
LOF
0.3261th %ile

The highest-scoring mechanism for this gene is dominant-negative.

DNprediction above median · 1 literature citation

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.

Literature Evidence

DNMMD-associated SNPs encode proteins with decreased E3 activity, and the most frequent MMD allele, RNF213 R4810K , is a dominant-negative mutant that decreases ubiquitylation globally.PMID:35135845

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

ClinVar Variant Classifications

898 submitted variants in ClinVar

Classification Summary

Pathogenic15
Likely Pathogenic12
VUS345
Likely Benign271
Benign147
Conflicting26
15
Pathogenic
12
Likely Pathogenic
345
VUS
271
Likely Benign
147
Benign
26
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
5
10
0
15
Likely Pathogenic
2
9
1
0
12
VUS
8
289
46
2
345
Likely Benign
1
74
45
151
271
Benign
1
53
30
63
147
Conflicting
26
Total12430132216816

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

View in ClinVar →

Protein Context — Lollipop Plot

RNF213 · 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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