GLRX3

Chr 10

glutaredoxin 3

Also known as: GLRX4, GRX3, GRX4, PICOT, TXNL2, TXNL3

This protein functions as a cytosolic iron-sulfur cluster assembly factor that facilitates [2Fe-2S] cluster insertion into cytosolic proteins and is required for hemoglobin maturation. Mutations cause autosomal recessive myopathy with lactic acidosis and sideroblastic anemia, typically presenting in infancy with severe anemia and muscle weakness. The gene shows moderate constraint against loss-of-function variants (LOEUF 0.477), reflecting its essential role in cellular iron-sulfur metabolism.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
3
Pubs (1 yr)
97
P/LP submissions
0%
P/LP missense
0.48
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryGLRX3
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.23) despite low pLI — interpret in context.
📋
ClinVar Variants
97 unique Pathogenic / Likely Pathogenic· 54 VUS of 176 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.48LOEUF
pLI 0.358
Z-score 3.36
OE 0.23 (0.120.48)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
0.15Z-score
OE missense 0.97 (0.851.10)
157 obs / 162.3 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.23 (0.120.48)
00.351.4
Missense OE0.97 (0.851.10)
00.61.4
Synonymous OE0.88
01.21.6
LoF obs/exp: 5 / 22.0Missense obs/exp: 157 / 162.3Syn Z: 0.73
DN
0.6745th %ile
GOF
0.6443th %ile
LOF
0.3647th %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

176 submitted variants in ClinVar

Classification Summary

Pathogenic92
Likely Pathogenic5
VUS54
Likely Benign1
Benign1
92
Pathogenic
5
Likely Pathogenic
54
VUS
1
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
92
0
92
Likely Pathogenic
0
0
5
0
5
VUS
0
46
8
0
54
Likely Benign
0
1
0
0
1
Benign
0
0
0
1
1
Total0471051153

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

View in ClinVar →

Protein Context — Lollipop Plot

GLRX3 · 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 →