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Myosin, heavy chain 7, cardiac muscle, beta

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
Standing on the Shoulders of Giants: J.A.P. Paré and the Birth of Cardiovascular Genetics.
McKenna et al., London, United Kingdom. In Can J Cardiol, 30 Nov 2015
MYH7 was the first gene implicated in a cardiovascular disease, which paved the way for identification of mutations in other heritable disorders, mechanistic studies, and clinical applications, such as predictive testing.
Targeted next-generation sequencing of candidate genes reveals novel mutations in patients with dilated cardiomyopathy.
Xia et al., Kunming, China. In Int J Mol Med, 07 Nov 2015
The candidate genes that may cause DCM include MYBPC3, MYH6, MYH7, LMNA, TNNT2, TNNI3, MYPN, MYL3, TPM1, SCN5A, DES, ACTC1 and RBM20.
Comparative transcriptome analysis of atrial septal defect identify dysregulated genes during heart septum morphogenesis.
Jiang et al., Kunming, China. In Gene, 13 Oct 2015
The results indicated that cardiac specific transcriptional factors (GATA4 and NKX2-5), extracellular signal molecules (VEGFA and BMP10) and cardiac sarcomeric proteins (MYL2, MYL3, MYH7, TNNT1 and TNNT3) were downregulated in ASD which may affect heart atrial septum formation, cardiomyocyte proliferation and cardiac muscle development.
Intrauterine Treatment of a Fetus with Familial Hypertrophic Cardiomyopathy Secondary to MYH7 Mutation.
Barber et al., Tucson, United States. In Pediatr Cardiol, 04 Oct 2015
UNASSIGNED: There is no clear consensus on optimal management of fetuses affected by familial hypertrophic cardiomyopathy (HCM).
[MicroRNA-133a antagonizes phenylephrine-induced hypertrophy of neonatal rat cardiomyocytes in vitro].
Ma et al., Haikou, China. In Nan Fang Yi Ke Da Xue Xue Bao, Aug 2015
Neonatal rat cardiac myocytes treated by phenylephrine were exposed to miR-133a adenovirus, and the changes in cell area was measured; the expression levels of miR-133a and Acta1, Actc1, Actb, Myh6, Myh7, and BNP mRNAs were detected by quantitative RT-PCR.
OBSCN Mutations Associated with Dilated Cardiomyopathy and Haploinsufficiency.
Knöll et al., London, United Kingdom. In Plos One, Dec 2014
Also identified were 6 truncating mutations in TTN, 3 mutations in MYH7, 2 in DSP and one each in TNNC1, TNNI3, MYOM1, VCL, GLA, PLB, TCAP, PKP2 and LAMA4.
A long noncoding RNA protects the heart from pathological hypertrophy.
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.
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.
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.
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.
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.
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.
Udd et al., Italy. In Neuromuscul Disord, 2012
This study suggested that MYH7 mutation is related distal myopathy.
Mechanisms of disease: hypertrophic cardiomyopathy.
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.
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.
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.
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].
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.
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.
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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