USP53

Chr 4AR

ubiquitin specific peptidase 53

Also known as: PFIC7

USP53 encodes a deubiquitinase that cleaves K63-linked polyubiquitin chains from tight junction proteins, modulating barrier properties and mechanical stability of tight junctions. Mutations cause autosomal recessive progressive familial intrahepatic cholestasis type 7, which may be associated with hearing loss due to the protein's role in auditory hair cell survival. This gene is not highly constrained against loss-of-function variants.

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

Cholestasis, progressive familial intrahepatic, 7, with or without hearing lossMIM #619658
AR
0
Active trials
15
Pubs (1 yr)
82
P/LP submissions
8%
P/LP missense
0.78
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryUSP53
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
62 unique Pathogenic / Likely Pathogenic· 141 VUS of 300 total submissions
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GeneReview available — USP53
Authoritative clinical overview · Recommended first read
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Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.78LOEUF
pLI 0.000
Z-score 2.83
OE 0.57 (0.420.78)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.98Z-score
OE missense 0.88 (0.820.95)
496 obs / 561.5 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.57 (0.420.78)
00.351.4
Missense OE0.88 (0.820.95)
00.61.4
Synonymous OE0.87
01.21.6
LoF obs/exp: 29 / 50.7Missense obs/exp: 496 / 561.5Syn Z: 1.41
DN
0.6743th %ile
GOF
0.6151th %ile
LOF
0.4332th %ile

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative and loss-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
LOF39% of P/LP variants are LoF

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. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

300 submitted variants in ClinVar

Classification Summary

Pathogenic39
Likely Pathogenic23
VUS141
Likely Benign47
Benign22
Conflicting7
39
Pathogenic
23
Likely Pathogenic
141
VUS
47
Likely Benign
22
Benign
7
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
12
2
25
0
39
Likely Pathogenic
12
3
8
0
23
VUS
1
130
9
1
141
Likely Benign
0
10
13
24
47
Benign
0
9
5
8
22
Conflicting
7
Total251546033279

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

View in ClinVar →

Protein Context — Lollipop Plot

USP53 · 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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