MYH2

Chr 17ADAR

myosin heavy chain 2

Also known as: CMYO6, CMYP6, IBM3, MYH2A, MYHSA2, MYHas8, MyHC-2A, MyHC-IIa

The MYH2 gene encodes a class II myosin heavy chain that functions as an actin-based motor protein essential for skeletal muscle contraction. Mutations cause congenital myopathy 6 with ophthalmoplegia through a dominant-negative mechanism, inherited in both autosomal dominant and autosomal recessive patterns. The protein localizes to myofibrils in the cytoplasm and is part of heterohexameric muscle myosin complexes that generate mechanical force for muscle function.

OMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
MultiplemechanismAD/ARLOEUF 0.691 OMIM phenotype
Clinical SummaryMYH2
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Gene-Disease Validity (ClinGen)
myopathy, proximal, and ophthalmoplegia · ADModerate

Moderate evidence — consider for supplementary testing

2 total gene-disease associations curated

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
15 unique Pathogenic / Likely Pathogenic· 112 VUS of 200 total submissions
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Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.69LOEUF
pLI 0.000
Z-score 4.15
OE 0.55 (0.440.69)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
1.97Z-score
OE missense 0.82 (0.780.87)
826 obs / 1001.7 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.55 (0.440.69)
00.351.4
Missense OE0.82 (0.780.87)
00.61.4
Synonymous OE1.04
01.21.6
LoF obs/exp: 53 / 97.1Missense obs/exp: 826 / 1001.7Syn Z: -0.69
DN
0.89top 5%
GOF
0.7127th %ile
LOF
0.2091th %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 · 1 literature citation
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.

Literature Evidence

DNBecause it is known that the expression of MyHC IIa increases with age this observation explains the progressive course of the disease in adulthood and confirms the dominant negative effect of the p.E706K mutation.PMID:23489661

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

200 submitted variants in ClinVar

Classification Summary

Pathogenic6
Likely Pathogenic9
VUS112
Likely Benign66
Benign1
Conflicting6
6
Pathogenic
9
Likely Pathogenic
112
VUS
66
Likely Benign
1
Benign
6
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
5
0
1
0
6
Likely Pathogenic
9
0
0
0
9
VUS
1
105
6
0
112
Likely Benign
0
0
26
40
66
Benign
0
0
0
1
1
Conflicting
6
Total151053341200

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

View in ClinVar →

Protein Context — Lollipop Plot

MYH2 · protein map & ClinVar variants

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

3D Protein StructureAlphaFold
Clinical Literature
Open Research Assistant →
Key Publications
Landmark & review papers · by relevance
PubMed
Top 5 results · since 2015Search PubMed ↗