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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
L-arginine Attenuates Cardiac Dysfunction, but further Down-Regulates Alpha Myosin Heavy Chain Expression in Isoproterenol-Induced Cardiomyopathy.
New
Krenek et al., Bratislava, Slovakia. In Basic Clin Pharmacol Toxicol, 10 May 2015
RT-PCR showed increased mRNA levels of cardiac hypertrophy marker ANP, but not BNP, decreased expression of myosin heavy chain isoform MYH6, unaltered expression of pathological MYH7.
Dual LQT1 and HCM phenotypes associated with tetrad heterozygous mutations in KCNQ1, MYH7, MYLK2, and TMEM70 genes in a three-generation Chinese family.
New
Liu et al., Xi'an, China. In Europace, 29 Apr 2015
These were two novel MYH7-H1717Q and MYLK2-K324E mutations accompanied by the KCNQ1-R190W and TMEM70-I147T mutations.
New cardiac and skeletal protein aggregate myopathy associated with combined MuRF1 and MuRF3 mutations.
New
Tajsharghi et al., Barcelona, Spain. In Hum Mol Genet, 23 Apr 2015
Sanger sequencing excluded mutations in the MSM-associated gene MYH7 but identified mutations in TRIM63 and TRIM54, encoding MuRF1 and MuRF3, respectively.
Heterogeneous activation of a slow myosin gene in proliferating myoblasts and differentiated single myofibers.
New
Kuang et al., West Lafayette, United States. In Dev Biol, 17 Apr 2015
Lineage tracing indicates that during development all muscles have activated the fast myosin gene Myl1, but not the slow myosin gene Myh7, which is activated in all slow but a subset of fast myofibers.
Experimental heart failure modelled by the cardiomyocyte-specific loss of an epigenome modifier, DNMT3B.
New
Foo et al., Cambridge, United Kingdom. In J Mol Cell Cardiol, 14 Apr 2015
By targeted candidate gene quantitative RT-PCR, we discovered an over-activity of cryptic splice sites in the sarcomeric gene Myh7, resulting in a transcript with 8 exons missing.
MicroRNA-223 Displays a Protective Role Against Cardiomyocyte Hypertrophy by Targeting Cardiac Troponin I-Interacting Kinase.
New
Li et al., Shanghai, China. In Cell Physiol Biochem, Dec 2014
MiR-223 overexpression in CMs alleviated ET-1 induced hypertrophy, evidenced by smaller cell surface area and downregulated ANP, α-actinin, Myh6 and Myh7 expression.
A long noncoding RNA protects the heart from pathological hypertrophy.
New
Impact
Chang et al., Indianapolis, United States. In Nature, 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.
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.
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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