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Myosin, heavy chain 7, cardiac muscle, beta

MYH7
Muscle myosin is a hexameric protein containing 2 heavy chain subunits, 2 alkali light chain subunits, and 2 regulatory light chain subunits. This gene encodes the beta (or slow) heavy chain subunit of cardiac myosin. It is expressed predominantly in normal human ventricle. It is also expressed in skeletal muscle tissues rich in slow-twitch type I muscle fibers. Changes in the relative abundance of this protein and the alpha (or fast) heavy subunit of cardiac myosin correlate with the contractile velocity of cardiac muscle. Its expression is also altered during thyroid hormone depletion and hemodynamic overloading. Mutations in this gene are associated with familial hypertrophic cardiomyopathy, myosin storage myopathy, dilated cardiomyopathy, and Laing early-onset distal myopathy. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: cTnT, HAD, AGE, CAN, myosin light chain 2
Papers on MYH7
The association between brain natriuretic peptide and tissue Doppler parameters in children with hypertrophic cardiomyopathy.
New
Tavli et al., İzmir, Turkey. In Bosn J Basic Med Sci, Feb 2016
We performed electrocardiography, transthoracic echocardiography, and tissue Doppler echocardiography in each group, as well as genetic tests (for Arg403Gln, Arg453Cys, Arg719Trp and Arg719Gln mutations in MYH7 Exons 13, 14, 19) and BNP in the patients.
The Ups and Downs of Genetic Diagnosis of Hypertrophic Cardiomyopathy.
New
Coto et al., Oviedo, Spain. In Rev Esp Cardiol (engl), Jan 2016
In hypertrophic cardiomyopathy, genetic analysis has increased from the 3 main genes implicated in the disease (MYH7, MYBPC3, TNNT2) to sequencing of more than 20 related genes.
Myosin Content of Individual Human Muscle Fibers Isolated by Laser Capture Microdissection.
New
Stone et al., United States. In Am J Physiol Cell Physiol, Jan 2016
Fast-twitch (type IIx) fibers consistently contained myosin heavy chains 1, 2, and 4 and myosin light chain 1. Type I fibers always contained myosin heavy chains 6 and 7 (MYH6 and MYH7) and myosin light chain 3 (MYL3), whereas MYH6, MYH7, and MYL3 were nearly absent from IIx fibers.
De novo exonic mutation in MYH7 gene leading to exon skipping in a patient with early onset muscular weakness and fiber-type disproportion.
New
Reimand et al., Tartu, Estonia. In Neuromuscul Disord, Jan 2016
UNASSIGNED: Here we report on a case of MYH7-related myopathy in a boy with early onset of muscular weakness and delayed motor development in infancy.
The genetic basis of hypertrophic cardiomyopathy in cats and humans.
Review
New
Harris et al., Davis, United States. In J Vet Cardiol, Dec 2015
In people with HCM, the two most common genes affected by HCM mutations are the myosin heavy chain gene (MYH7), the gene that encodes for the motor protein β-myosin heavy chain (the sarcomeric protein that splits ATP to generate force), and the cardiac myosin binding protein-C gene (MYBPC3), a gene that encodes for the closely related structural and regulatory protein, cardiac myosin binding protein-C (cMyBP-C).
Electrical Stimulation Promotes Cardiac Differentiation of Human Induced Pluripotent Stem Cells.
New
Lim et al., Australia. In Stem Cells Int, Dec 2015
Acute electrical stimulation also significantly increased the cardiac gene expression of ACTC1, TNNT2, MYH7, and MYL7.
Genetic profile of hypertrophic cardiomyopathy in Tunisia: Is it different?
Olivotto et al., Monastir, Tunisia. In Glob Cardiol Sci Pract, 2014
Using the Illumina platform, a panel of 12 genes was analyzed including myosin binding protein C (MYBPC3), beta-myosin heavy chain (MYH7), regulatory and essential light chains (MYL2 and MYL3), troponin-T (TNNT2), troponin-I (TNNI3), troponin-C (TNNC1), alpha-tropomyosin (TPM1), alpha-actin (ACTC1), alpha-actinin-2 (ACTN2) as well as alfa-galactosidase (GLA), 5'-AMP-activated protein (PKRAG2), transthyretin (TTR) and lysosomal-associated membrane protein-2 (LAMP2) for exclusion of phenocopies.
A long noncoding RNA protects the heart from pathological hypertrophy.
Impact
Chang et al., Indianapolis, United States. In Nature, 2014
An estimated 70% of mouse genes undergo antisense transcription, including myosin heavy chain 7 (Myh7), which encodes molecular motor proteins for heart contraction.
A systematic review and meta-analysis of genotype-phenotype associations in patients with hypertrophic cardiomyopathy caused by sarcomeric protein mutations.
Review
Elliott et al., London, United Kingdom. In Heart, 2013
There were no differences when the two most frequently affected genes, MYBPC3 and MYH7, were compared.
Ebstein anomaly associated with left ventricular noncompaction: an autosomal dominant condition that can be caused by mutations in MYH7.
Review
Keavney et al., Amsterdam, Netherlands. In Am J Med Genet C Semin Med Genet, 2013
Recent studies identified mutations in the MYH7 gene, encoding the sarcomeric β-myosin heavy chain protein, in patients harboring this specific phenotype.
Abnormal calcium handling properties underlie familial hypertrophic cardiomyopathy pathology in patient-specific induced pluripotent stem cells.
Impact
Wu et al., Stanford, United States. In Cell Stem Cell, 2013
To elucidate the mechanisms underlying HCM development, we generated patient-specific induced pluripotent stem cell cardiomyocytes (iPSC-CMs) from a ten-member family cohort carrying a hereditary HCM missense mutation (Arg663His) in the MYH7 gene.
Genetic mutations and mechanisms in dilated cardiomyopathy.
Review
Puckelwartz et al., Chicago, United States. In J Clin Invest, 2013
Mutations in the genes encoding the thick filament components myosin heavy chain and myosin binding protein C (MYH7 and MYBPC3) together explain 75% of inherited HCMs, leading to the observation that HCM is a disease of the sarcomere.
Myosinopathies: pathology and mechanisms.
Review
Oldfors et al., Göteborg, Sweden. In Acta Neuropathol, 2013
Myopathies with scapuloperoneal, distal or limb-girdle muscle weakness including entities, such as myosin storage myopathy and Laing distal myopathy are the result of usually dominant mutations in the gene for slow/β cardiac MyHC (MYH7).
New phenotype and pathology features in MYH7-related distal myopathy.
GeneRIF
Udd et al., Italy. In Neuromuscul Disord, 2012
This study suggested that MYH7 mutation is related distal myopathy.
A low prevalence of MYH7/MYBPC3 mutations among familial hypertrophic cardiomyopathy patients in India.
GeneRIF
Narasimhan et al., Hyderābād, India. In Mol Cell Biochem, 2012
Four novel mutations in MYBPC3 and one in MYH7 were identified among familial hypertrophic cardiomyopathy patients in India
Unequal allelic expression of wild-type and mutated β-myosin in familial hypertrophic cardiomyopathy.
GeneRIF
Kraft et al., Hannover, Germany. In Basic Res Cardiol, 2011
mutation-specific allelic imbalance in the beta-myosin heavy chain represents a new pathogenic factor for Familial hypertrophic cardiomyopathy.
β-myosin heavy chain is induced by pressure overload in a minor subpopulation of smaller mouse cardiac myocytes.
GeneRIF
Simpson et al., San Francisco, United States. In Circ Res, 2011
After transverse aortic constriction hypertrophied myocytes contain no beta-myosin heavy chain (betaMyHC), only alpha-MyHC, identifying a new subpopulation of smaller working ventricular myocytes with more myosin.
[Mutation analysis of beta myosin heavy chain gene in hypertrophic cardiomyopathy families].
GeneRIF
Liang et al., Beijing, China. In Zhonghua Yi Xue Yi Chuan Xue Za Zhi, 2011
gene mutations of beta-myosin heavy chain gene (MYH7) in Chinese pedigrees with hypertrophic cardiomyopathy
Chromatin regulation by Brg1 underlies heart muscle development and disease.
Impact
Chang et al., Stanford, United States. In Nature, 2010
Adult cardiomyocytes in mice primarily express alpha-myosin heavy chain (alpha-MHC, also known as Myh6), whereas embryonic cardiomyocytes express beta-MHC (also known as Myh7).
Shared genetic causes of cardiac hypertrophy in children and adults.
Impact
Seidman et al., Boston, United States. In N Engl J Med, 2008
We sequenced eight genes: MYH7, MYBPC3, TNNT2, TNNI3, TPM1, MYL3, MYL2, and ACTC.
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