MYH3

Chr 17ADAR

myosin heavy chain 3

Also known as: CPSFS1A, CPSFS1B, CPSKF1A, CPSKF1B, DA2A, DA2B, DA2B3, DA8

The MYH3 protein is a contractile protein that converts chemical energy into mechanical energy through ATP hydrolysis and is essential for muscle function. Mutations cause multiple arthrogryposis syndromes including Freeman-Sheldon syndrome, Sheldon-Hall syndrome, and contractures-pterygia-spondylocarpotarsal fusion syndrome through dominant-negative mechanisms. These conditions follow autosomal dominant inheritance, though autosomal recessive inheritance has also been reported.

OMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
LOFmechanismAD/ARLOEUF 0.634 OMIM phenotypes
Clinical SummaryMYH3
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.63LOEUF
pLI 0.000
Z-score 4.70
OE 0.50 (0.400.63)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
1.74Z-score
OE missense 0.85 (0.800.90)
855 obs / 1011.1 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.50 (0.400.63)
00.351.4
Missense OE0.85 (0.800.90)
00.61.4
Synonymous OE1.06
01.21.6
LoF obs/exp: 51 / 102.2Missense obs/exp: 855 / 1011.1Syn Z: -0.97
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
strongMYH3-related spondylocarpotarsal synostosis syndromeLOFAR
definitiveMYH3-related distal arthrogryposisOTHERAD
DN
0.88top 5%
GOF
0.6540th %ile
LOF
0.2288th %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

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

MYH3 · protein map & ClinVar variants

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

3D Protein StructureAlphaFold

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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