IRX5

Chr 16AR

iroquois homeobox 5

Also known as: HMMS, IRX-2a, IRXB2

IRX5 encodes a transcription factor that establishes cardiac repolarization gradients by repressing potassium channel gene expression, promotes retinal cone bipolar cell differentiation, and regulates craniofacial and gonadal development through control of cell migration. Loss-of-function mutations cause Hamamy syndrome, an autosomal recessive disorder. The gene is highly intolerant to loss-of-function variants, supporting haploinsufficiency as the pathogenic mechanism.

Summary from RefSeq, OMIM, UniProt, Mechanism

Primary Disease Associations & Inheritance

Hamamy syndromeMIM #611174
AR
0
Active trials
11
Pubs (1 yr)
23
P/LP submissions
14%
P/LP missense
0.30
LOEUF· LoF intol.
LOF
Mechanism· predicted
Clinical SummaryIRX5
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Gene-Disease Validity (ClinGen)
craniofacial dysplasia - osteopenia syndrome · ARModerate

Moderate evidence — consider for supplementary testing

Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 0.97). One damaged copy is likely sufficient to cause disease.
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ClinVar Variants
21 unique Pathogenic / Likely Pathogenic· 97 VUS of 163 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.30LOEUF
pLI 0.975
Z-score 3.44
OE 0.06 (0.020.30)
Highly constrained

Highly LoF-intolerant (top ~10% of genes)

Missense Constraint
0.83Z-score
OE missense 0.86 (0.770.96)
232 obs / 270.4 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.06 (0.020.30)
00.351.4
Missense OE0.86 (0.770.96)
00.61.4
Synonymous OE1.16
01.21.6
LoF obs/exp: 1 / 15.7Missense obs/exp: 232 / 270.4Syn Z: -1.42
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
strongIRX5-related hypertelorism, severe, with midface prominence, myopia, intellectual developmental disorder, and bone fragilityOTHERAR

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

DN
0.4190th %ile
GOF
0.2696th %ile
LOF
0.81top 5%

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

ClinVar Variant Classifications

163 submitted variants in ClinVar

Classification Summary

Pathogenic20
Likely Pathogenic1
VUS97
Likely Benign35
Benign8
Conflicting1
20
Pathogenic
1
Likely Pathogenic
97
VUS
35
Likely Benign
8
Benign
1
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
1
3
16
0
20
Likely Pathogenic
0
0
1
0
1
VUS
1
91
5
0
97
Likely Benign
0
3
0
32
35
Benign
0
2
4
2
8
Conflicting
1
Total2992634162

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

View in ClinVar →

Protein Context — Lollipop Plot

IRX5 · 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 →
Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
PubTator3
Top 5 full-text resultsSearch PubTator3 ↗
Key Publications
Landmark & review papers · by relevance
PubMed
Top 5 results · since 2015Search PubMed ↗