PAX3

Chr 2ADSomaticAR

paired box 3

Also known as: CDHS, HUP2, PAX-3, WS1, WS3

This transcription factor contains a paired box domain and homeodomain and regulates cell proliferation, migration, and apoptosis during neural development and myogenesis. Mutations cause Waardenburg syndrome types 1 and 3 (characterized by congenital hearing loss and pigmentary abnormalities), craniofacial-deafness-hand syndrome, and alveolar rhabdomyosarcoma through both germline and somatic mechanisms. The gene follows autosomal dominant inheritance for the syndromic conditions and autosomal recessive inheritance for some presentations.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
LOFmechanismAD/Somatic/ARLOEUF 0.474 OMIM phenotypes
Clinical SummaryPAX3
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Gene-Disease Validity (ClinGen)
Waardenburg syndrome · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.24) despite low pLI — interpret in context.
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Clinical Trials
2 active or recruiting trials — potential therapeutic options may be available
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GeneReview available — PAX3
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.47LOEUF
pLI 0.241
Z-score 3.51
OE 0.24 (0.130.47)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
1.62Z-score
OE missense 0.73 (0.650.82)
206 obs / 282.5 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.24 (0.130.47)
00.351.4
Missense OE0.73 (0.650.82)
00.61.4
Synonymous OE1.08
01.21.6
LoF obs/exp: 6 / 24.9Missense obs/exp: 206 / 282.5Syn Z: -0.68
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitivePAX3-related craniofacial-deafness-hand syndromeLOFAD
moderatePAX3-related Waardenburg syndrome (biallelic)OTHERAR
definitivePAX3-related Waardenburg syndrome (monoallelic)LOFAD
DN
0.73top 25%
GOF
0.5170th %ile
LOF
0.56top 25%

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative, loss-of-function 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 · 1 literature citation
LOF1 literature citation · LOEUF 0.47
GOF1 literature citation

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.

Literature Evidence

DNHeterozygous mutations could either reflect a unique dominant-negative effect or possibly the contribution of other unlinked genetic modifiers in determining the phenotype.PMID:11683776
GOFThe transcriptional activator PAX3-FKHR rescues the defects of Pax3 mutant mice but induces a myogenic gain-of-function phenotype with ligand-independent activation of Met signaling in vivoPMID:14665670
LOFWaardenburg's syndrome patients have mutations in the human homologue of the Pax-3 paired box genePMID:1347148

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

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

PAX3 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold
Clinical Literature
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