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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, ACID
Papers on MYH7
Caffeine Exposure Alters Cardiac Gene Expression in Embryonic Cardiomyocytes.
New
Wendler et al., United States. In Am J Physiol Regul Integr Comp Physiol, 29 Nov 2014
In HL-1 and primary embryonic cardiomyocytes, caffeine treatment for 48 hours significantly altered the expression of cardiac structural genes (Myh6, Myh7, Myh7b, Tnni3), hormonal genes (Anp and BnP), cardiac transcription factors (Gata4, Mef2c, Mef2d, Nfatc1), and microRNAs (miRNAs; miR208a, miR208b, miR499).
Proteomic Analysis of Human Fetal Atria and Ventricle.
New
Gramolini et al., In J Proteome Res, 17 Nov 2014
Several previously characterised cardiac chamber-enriched proteins were identified in this study including atrial isoform of myosin light chain 2 (MYL7), atrial natriuretic peptide (NPPA), connexin 40 (GJA5), and peptidylglycine alpha-amidating monooxygenase (PAM) for atria, and ventricular isoforms of myosin light chains (MYL2 and MYL3), myosin heavy chain 7 (MYH7), and connexin 43 (GJA1) for ventricle.
A long noncoding RNA protects the heart from pathological hypertrophy.
New
Impact
Chang et al., Indianapolis, United States. In Nature, 02 Nov 2014
An estimated 70% of mouse genes undergo antisense transcription, including myosin heavy chain 7 (Myh7), which encodes molecular motor proteins for heart contraction.
[Pro731Ser mutation in the β-myosin heavy chain and hypertrophic cardiomyopathy in a Chinese pedigree].
New
Wang et al., Qingdao, China. In Zhonghua Xin Xue Guan Bing Za Zhi, Jul 2014
RESULTS: A missense mutation (c.2191C > T, p. Pro731Ser) in the 20th exon of MYH7 gene was identified.
Hypothesis and theory: mechanical instabilities and non-uniformities in hereditary sarcomere myopathies.
New
Månsson, Kalmar, Sweden. In Front Physiol, Dec 2013
Similar mutations in skeletal muscle, e.g., in the MYH7 gene for slow myosin found in both the cardiac ventricle and slow skeletal muscle, may also cause severe disease but the severity and the morphological changes are often different.
A systematic review and meta-analysis of genotype-phenotype associations in patients with hypertrophic cardiomyopathy caused by sarcomeric protein mutations.
Review
New
Elliott et al., London, United Kingdom. In Heart, Dec 2013
There were no differences when the two most frequently affected genes, MYBPC3 and MYH7, were compared.
Familial hypertrophic cardiomyopathy: functional variance among individual cardiomyocytes as a trigger of FHC-phenotype development.
New
Kraft et al., Hannover, Germany. In Front Physiol, Dec 2013
Here we show for different MYH7 mutations variance in force pCa-relations from normal to highly abnormal as a feature common to all mutations we studied, while direct functional effects of the different FHC-mutations, e.g., on force generation, ATPase or calcium sensitivity of the contractile system, can be quite different.
Potential genetic predisposition for anthracycline-associated cardiomyopathy in families with dilated cardiomyopathy.
New
van den Berg et al., Groningen, Netherlands. In Open Heart, Dec 2013
Pathogenic MYH7 mutations were identified in two of these six families.
Ebstein anomaly associated with left ventricular noncompaction: an autosomal dominant condition that can be caused by mutations in MYH7.
Review
New
Keavney et al., Amsterdam, Netherlands. In Am J Med Genet C Semin Med Genet, Aug 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.
New
Impact
Wu et al., Stanford, United States. In Cell Stem Cell, Feb 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
New
Puckelwartz et al., Chicago, United States. In J Clin Invest, Feb 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.
Mechanisms of disease: hypertrophic cardiomyopathy.
Review
Katus et al., Kiel, Germany. In Nat Rev Cardiol, 2012
Interestingly, most of these genes encode sarcomeric proteins, such as myosin-7 (also known as cardiac muscle β-myosin heavy chain; MYH7), cardiac myosin-binding protein C (MYBPC3), and cardiac muscle troponin T (TNNT2).
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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