TXNL4A

Chr 18AR

thioredoxin like 4A

Also known as: BMKS, DIB1, DIM1, SNRNP15, TXNL4, U5-15kD

The encoded protein is a component of the U5 small ribonucleoprotein particle that functions in pre-mRNA splicing as part of spliceosome assembly and the precatalytic spliceosome B complex. Mutations cause Burn-McKeown syndrome, a rare autosomal recessive disorder characterized by craniofacial dysmorphisms, cardiac defects, hearing loss, and bilateral choanal atresia. The gene shows low constraint against loss-of-function variants (pLI ~0, LOEUF 1.8), consistent with the recessive inheritance pattern.

Summary from RefSeq, OMIM, UniProt
Research Assistant →

Primary Disease Associations & Inheritance

Burn-McKeown syndromeMIM #608572
AR
0
Active trials
3
Pubs (1 yr)
201
P/LP submissions
0%
P/LP missense
1.82
LOEUF
LOF
Mechanism· G2P
Clinical SummaryTXNL4A
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Gene-Disease Validity (ClinGen)
choanal atresia-hearing loss-cardiac defects-craniofacial dysmorphism syndrome · ARDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
178 unique Pathogenic / Likely Pathogenic· 29 VUS of 231 total submissions
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GeneReview available — TXNL4A
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.82LOEUF
pLI 0.000
Z-score -0.15
OE 1.07 (0.571.82)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
2.77Z-score
OE missense 0.17 (0.110.26)
15 obs / 88.2 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE1.07 (0.571.82)
00.351.4
Missense OE0.17 (0.110.26)
00.61.4
Synonymous OE1.20
01.21.6
LoF obs/exp: 6 / 5.6Missense obs/exp: 15 / 88.2Syn Z: -0.89
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveTXNL4A-related Burn Mckeown syndromeLOFAR

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

DN
0.6744th %ile
GOF
0.6736th %ile
LOF
0.3259th %ile

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.

ClinVar Variant Classifications

231 submitted variants in ClinVar

Classification Summary

Pathogenic166
Likely Pathogenic12
VUS29
Likely Benign7
Benign12
166
Pathogenic
12
Likely Pathogenic
29
VUS
7
Likely Benign
12
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
2
0
164
0
166
Likely Pathogenic
2
0
10
0
12
VUS
1
10
18
0
29
Likely Benign
0
0
4
3
7
Benign
0
0
11
1
12
Total5102074226

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

View in ClinVar →

Protein Context — Lollipop Plot

TXNL4A · 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
Open Research Assistant →
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC