RNF19A

Chr 8

ring finger protein 19A, RBR E3 ubiquitin protein ligase

Also known as: RNF19

The protein functions as an E3 ubiquitin ligase that targets specific substrates including synphilin-1 and pathogenic SOD1 variants for proteasomal degradation. Mutations cause autosomal recessive spastic paraplegia, which primarily affects the corticospinal tracts leading to progressive lower limb spasticity and weakness. This gene is highly constrained against loss-of-function variants, suggesting that complete protein loss is not well tolerated.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
4
Pubs (1 yr)
37
P/LP submissions
0%
P/LP missense
0.47
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryRNF19A
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.28) despite low pLI — interpret in context.
📋
ClinVar Variants
37 unique Pathogenic / Likely Pathogenic· 78 VUS of 134 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.47LOEUF
pLI 0.025
Z-score 4.00
OE 0.28 (0.170.47)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
2.38Z-score
OE missense 0.69 (0.630.76)
322 obs / 466.7 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.28 (0.170.47)
00.351.4
Missense OE0.69 (0.630.76)
00.61.4
Synonymous OE1.01
01.21.6
LoF obs/exp: 10 / 35.9Missense obs/exp: 322 / 466.7Syn Z: -0.06
DN
0.7130th %ile
GOF
0.7028th %ile
LOF
0.4628th %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

134 submitted variants in ClinVar

Classification Summary

Pathogenic36
Likely Pathogenic1
VUS78
Likely Benign2
Benign1
36
Pathogenic
1
Likely Pathogenic
78
VUS
2
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
36
0
36
Likely Pathogenic
0
0
1
0
1
VUS
0
72
6
0
78
Likely Benign
0
2
0
0
2
Benign
0
0
0
1
1
Total074431118

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

View in ClinVar →

Protein Context — Lollipop Plot

RNF19A · 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.

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Clinical Literature
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