Genomes and Genes
Gene Symbol: MYH7
Description: myosin heavy chain 7
Alias: CMD1S, CMH1, MPD1, MYHCB, SPMD, SPMM, myosin-7, cardiac muscle myosin heavy chain 7 beta, myHC-beta, myhc-slow, myopathy, distal 1, myosin 7, myosin heavy chain beta-subunit, myosin heavy chain slow isoform, myosin heavy chain, cardiac muscle beta isoform, myosin, heavy chain 7, cardiac muscle, beta, myosin, heavy polypeptide 7, cardiac muscle, beta, rhabdomyosarcoma antigen MU-RMS-40.7A
Publications264 found, 100 shown here
- Mutation screening in dilated cardiomyopathy: prominent role of the beta myosin heavy chain geneEric Villard
INSERM Unité 621, IFR14, CIB Pitié Salpêtrière, 91 Bd de l Hopital, 75013 Paris, France
Eur Heart J 26:794-803. 2005..Here, we performed a mutation analysis of four genes involved in FDCM in a population of idiopathic DCM...
- A 7.1 kbp beta-myosin heavy chain promoter, efficient for green fluorescent protein expression, probably induces lethality when overexpressing a mutated transforming growth factor-beta type II receptor in transgenic miceSeverine Allegra
UMR 369 INSERM UCBL and IFR 62 Laënnec
Transgenic Res 14:69-80. 2005..Analysis of the consequences of the blocking of the TGFbeta signalling pathway in the heart will require the use of tissue specific means of conditional gene invalidation...
- Activation of the beta myosin heavy chain promoter by MEF-2D, MyoD, p300, and the calcineurin/NFATc1 pathwayJoachim D Meissner
Department of Physiology, Hannover Medical School, Hannover, Germany
J Cell Physiol 211:138-48. 2007..Together, our findings demonstrate calcium-ionophore-induced activation of the beta MyHC promoter by NFATc1, MyoD, MEF-2D, and p300 in a calcineurin-dependent manner...
- Characteristics and prognostic implications of myosin missense mutations in familial hypertrophic cardiomyopathyH Watkins
Cardiology Division, Brigham and Women s Hospital, Boston, MA
N Engl J Med 326:1108-14. 1992..However, neither the proportion of cases attributable to myosin mutations nor the effects of different mutations on clinical outcome are known...
- A molecular basis for familial hypertrophic cardiomyopathy: a beta cardiac myosin heavy chain gene missense mutationA A Geisterfer-Lowrance
Cardiovascular Division, Brigham and Women s Hospital, Boston, Massachusetts 02115
Cell 62:999-1006. 1990..The pathology resulting from a missense mutation at residue 403 further suggests that a critical function of myosin is disrupted by this mutation...
- Molecular cloning and characterization of human cardiac alpha- and beta-form myosin heavy chain complementary DNA clones. Regulation of expression during development and pressure overload in human atriumM Kurabayashi
Third Department of Internal Medicine, University of Tokyo, Japan
J Clin Invest 82:524-31. 1988..Finally, we demonstrate that MHC isozymic transition in pressure-overloaded atrium is, at least in part, regulated at a pretranslational level...
- Structural interpretation of the mutations in the beta-cardiac myosin that have been implicated in familial hypertrophic cardiomyopathyI Rayment
Institute for Enzyme Research, Graduate School, University of Wisconsin, Madison 53705 4098, USA
Proc Natl Acad Sci U S A 92:3864-8. 1995..kindreds, the disease is caused by > 29 missense mutations in the cardiac beta-myosin heavy chain (MYH7) gene...
- Independent origin of identical beta cardiac myosin heavy-chain mutations in hypertrophic cardiomyopathyH Watkins
Cardiology Division, Brigham and Women s Hospital, Boston, MA
Am J Hum Genet 53:1180-5. 1993..This finding predicts the prevalence of disease-causing beta cardiac MHC mutations to be comparable in all population groups...
- Familial hypertrophic cardiomyopathy. Microsatellite haplotyping and identification of a hot spot for mutations in the beta-myosin heavy chain geneE Dausse
Institut National de la Sante et de la Recherche Medicale, U127, Hopital Lariboisiere, Paris, France
J Clin Invest 92:2807-13. 1993..Our results also indicate that codon 403 of the beta-myosin heavy chain gene is a hot spot for mutations causing FHC...
- Prognostic implications of novel beta cardiac myosin heavy chain gene mutations that cause familial hypertrophic cardiomyopathyR Anan
Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115
J Clin Invest 93:280-5. 1994..Phe513Cys mutation (P < 0.001) support the hypothesis that mutations which alter the charge of the encoded amino acid affect survival more significantly than those that produce a conservative amino acid change...
- Missense mutations in the beta-myosin heavy-chain gene cause central core disease in hypertrophic cardiomyopathyL Fananapazir
Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892
Proc Natl Acad Sci U S A 90:3993-7. 1993..In less than half of kindreds with HCM, the disease is linked to the beta-myosin heavy-chain gene locus (MYH7)...
- Mutations in sarcomere protein genes as a cause of dilated cardiomyopathyM Kamisago
Cardiovascular Division, Brigham and Women s Hospital, and Harvard Medical School and Howard Hughes Medical Institute, Boston, MA, USA
N Engl J Med 343:1688-96. 2000..To elucidate this important cause of heart failure, we investigated other genetic causes of dilated cardiomyopathy...
- Malignant hypertrophic cardiomyopathy caused by the Arg723Gly mutation in beta-myosin heavy chain geneM Enjuto
Molecular Cardiology Laboratory, Laboratory of Clinical Biochemistry and the Cardiovascular Institute, Hospital Clinic IDIBAPS, University of Barcelona, Villarroel 170, Barcelona, 08036, Spain
J Mol Cell Cardiol 32:2307-13. 2000..Mean survival of affected members was 51 years. In conclusion, a new mutation Arg723Gly in beta-myosin heavy chain gene is reported which shortens life expectancy because of sudden death and end-stage heart failure...
- Beta-myosin heavy chain gene mutations and hypertrophic cardiomyopathy in Austrian childrenS Greber-Platzer
Department of Pediatrics, Division of Pediatric Cardiology, University of Vienna, Wahringer Gurtel 18 20, Vienna, A 1090, Austria
J Mol Cell Cardiol 33:141-8. 2001....
- Prevalence and severity of "benign" mutations in the beta-myosin heavy chain, cardiac troponin T, and alpha-tropomyosin genes in hypertrophic cardiomyopathySara L Van Driest
Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, Minn 55905, USA
Circulation 106:3085-90. 2002..associated with near-normal survival: N232S, G256E, F513C, V606M, R719Q, and L908V of beta-myosin heavy chain (MYH7); S179F of troponin T (TNNT2); and D175N of alpha-tropomyosin (TPM1)...
- Hypertrophic cardiomyopathy: distribution of disease genes, spectrum of mutations, and implications for a molecular diagnosis strategyPascale Richard
UF de Cardiogénétique et Myogénétique, Service de Biochimie B, Hopital de la Salpetriere, 47 Bld de l Hopital, 75651 Paris Cedex 13, France
Circulation 107:2227-32. 2003..The aim of the present study was to perform a systematic screening of these genes in a large population, to evaluate the distribution of the disease genes, and to determine the best molecular strategy in clinical practice...
- Mutation in myosin heavy chain 6 causes atrial septal defectYung Hao Ching
Institute of Genetics, University of Nottingham, Queen s Medical Centre, Nottingham NG7 2UH, UK
Nat Genet 37:423-8. 2005..These data provide evidence for a link between a transcription factor, a structural protein and congenital heart disease...
- Prevalence of cardiac beta-myosin heavy chain gene mutations in patients with hypertrophic cardiomyopathyAndreas Perrot
Kardiologie am Campus Buch und Virchow Klinikum, Charité Universitätsmedizin Berlin und Max Delbrück Centrum für Molekulare Medizin, Wiltbergstrasse 50, 13125 Berlin, Germany
J Mol Med (Berl) 83:468-77. 2005..Mutations in the cardiac beta-myosin heavy chain gene (MYH7) are responsible for the disease in about 30% of cases where mutations were identified...
- MYH7 gene mutation in myosin storage myopathy and scapulo-peroneal myopathyElena Pegoraro
Department of Neurosciences, University of Padova, Italy
Neuromuscul Disord 17:321-9. 2007In order to characterize, at the clinical, molecular and imaging level, myopathies due to MYH7 gene mutations, MYH7 gene analysis was conducted by RT-PCR/SSCP/sequencing in two patients diagnosed with myosin storage myopathy and 17 ..
- Troponin T and beta-myosin mutations have distinct cardiac functional effects in hypertrophic cardiomyopathy patients without hypertrophyMiriam Revera
Department of Cardiology, IRCCS San Matteo Hospital, Pavia, Italy
Cardiovasc Res 77:687-94. 2008..The aims of this study were to investigate whether distinct HCM-mutations have different consequences for cardiac structure and function in the absence of the confounding effects of hypertrophy...
- Familial hypertrophic cardiomyopathy associated with cardiac beta-myosin heavy chain and troponin I mutationsAisha Frazier
Department of Pediatrics, Cardiology Division, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA
Pediatr Cardiol 29:846-50. 2008..an individual with severe disease has alterations in two sarcomeric protein genes, cardiac beta-myosin heavy chain (MYH7) and troponin I (TNNI3). Each of her children has only one of these mutations...
- Bioinformatics assessment of beta-myosin mutations reveals myosin's high sensitivity to mutationsMassimo Buvoli
Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO 80309, USA
Trends Cardiovasc Med 18:141-9. 2008More than 200 mutations in the beta-myosin gene (MYH7) that cause clinically distinct cardiac and/or skeletal myopathies have been reported, but to date, no comprehensive statistical analysis of these mutations has been performed...
- Genotype phenotype correlations of cardiac beta-myosin heavy chain mutations in Indian patients with hypertrophic and dilated cardiomyopathyTaranjit Singh Rai
Department of Experimental Medicine and Biotechnology, Post Graduate Institute of Medical Education and Research, Chandigarh, India
Mol Cell Biochem 321:189-96. 2009The aim of the current study was to determine the frequency of mutations in the beta-myosin heavy chain gene (MYH7) in a cohort of hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) and their families, and to investigate ..
- Striking phenotypic variability in two familial cases of myosin storage myopathy with a MYH7 Leu1793pro mutationEmmanuelle Uro-Coste
Department of Pathology, Rangueil University Hospital, TSA 50032, 31059 Toulouse Cedex 9, France
Neuromuscul Disord 19:163-6. 2009..We have identified in a woman and her daughter, a pLeu1793Pro mutation in MYH7. This mutation has already been reported to be associated with MSM presenting as neonatal hypotony...
- MYH7 gene tail mutation causing myopathic profiles beyond Laing distal myopathyN Muelas
Department of Neurology, Hospital Universitario La Fe, Avda Campanar 21, 46009 Valencia, Spain
Neurology 75:732-41. 2010To describe a wide range of clinical and pathologic myopathic profiles associated with the p.K1729del mutation in the MYH7 gene, known to cause Laing distal myopathy.
- New phenotype and pathology features in MYH7-related distal myopathyGiorgio Tasca
Don Carlo Gnocchi ONLUS Foundation, Italy
Neuromuscul Disord 22:640-7. 2012..is an autosomal dominant disease due to mutations in the gene encoding for the human slow-β myosin heavy chain, MYH7. Most reports describe it as a mild, early onset myopathy with involvement usually restricted to foot extensors, ..
- Mutations in MYH7 cause Multi-minicore Disease (MmD) with variable cardiac involvementT Cullup
DNA Laboratory, GSTS Pathology, Guy s Hospital, London, UK
Neuromuscul Disord 22:1096-104. 2012..A proportion of cases remain unresolved. Mutations in MYH7 encoding the beta myosin heavy chain protein have been implicated in cardiac and, less frequently, skeletal muscle ..
- Molecular consequences of the R453C hypertrophic cardiomyopathy mutation on human β-cardiac myosin motor functionRuth F Sommese
Department of Biochemistry, Stanford University School of Medicine, Stanford, CA 94305, USA
Proc Natl Acad Sci U S A 110:12607-12. 2013..Loaded in vitro motility assay confirms that the net force in the ensemble is indeed increased. Overall, this study suggests that the R453C mutation should result in a hypercontractile state in the heart muscle. ..
- The complete sequence of the human beta-myosin heavy chain gene and a comparative analysis of its productT Jaenicke
Max Planck Institut for Medical Research, Department of Cell Physiology, Heidelberg, Federal Republic of Germany
Genomics 8:194-206. 1990..We have isolated and sequenced the gene and the cDNA coding for the human cardiac beta-myosin heavy chain (designated MYH7). The gene is 22,883 bp long. The 1935 amino acids of this protein (Mr223,111) are encoded by 38 exons...
- The origins of hypertrophic cardiomyopathy-causing mutations in two South African subpopulations: a unique profile of both independent and founder eventsJ C Moolman-Smook
US MRC Centre for Molecular and Cellular Biology, Department of Medical Biochemistry, University of Stellenbosch Medical School, Tygerberg, South Africa
Am J Hum Genet 65:1308-20. 1999..The milder phenotype of the betaMHC mutations may account for the presence of these founder effects, whereas population dynamics alone may have overridden the reproductive disadvantage incurred by the more lethal, cTnT Arg92Trp mutation...
- Cardiomyopathy mutations reveal variable region of myosin converter as major element of cross-bridge complianceB Seebohm
Molecular and Cell Physiology, Medical School, Hannover, Germany
Biophys J 97:806-24. 2009..Because amino acids 719 and 723 are nonconserved residues, cross-bridge stiffness may well be specifically tuned for different myosins...
- [Demonstration of a fifth locus implicated in familial hypertrophic cardiomyopathies]C Hengstenberg
INSERM U153, , Paris
Arch Mal Coeur Vaiss 87:1655-62. 1994..There is, therefore, a fifth gene implicated in familial HCM. The heterogeneity of the disease seems even greater than originally thought...
- The influence of dietary salt and plasma renin activity on myosin heavy chain gene expression in rat heartsP Buttrick
Montefiore Medical Center, Bronx, NY 10467
Am J Hypertens 6:579-85. 1993..However, sodium restriction, either via its hemodynamic or humoral effects, is sufficient to induce a physiologic change in myosin heavy chain gene expression in rats...
- Activity of the beta-myosin heavy chain antisense promoter responds to diabetes and hypothyroidismJulia Giger
Department of Physiology and Biophysics, University of California, Irvine, D 346, Med Sci I, Irvine, CA 92697, USA
Am J Physiol Heart Circ Physiol 292:H3065-71. 2007..We conclude that there is an intergenic promoter that is active in the AS direction and that the putative RAR element is a vital regulatory site...
- Hypertrophic cardiomyopathy: low frequency of mutations in the beta-myosin heavy chain (MYH7) and cardiac troponin T (TNNT2) genes among Spanish patientsMonica Garcia-Castro
Genética Molecular Instituto de Investigación Nefrológica IRSIN FRIAT and Servicio de Cardiología, Hospital Central de Asturias, 33006 Oviedo, Spain
Clin Chem 49:1279-85. 2003Mutations in the cardiac beta-myosin heavy chain (MYH7) and cardiac troponin T (TNNT2) genes are reportedly responsible for up to 40% of familial cases with hypertrophic cardiomyopathy (HC)...
- Simvastatin induces regression of cardiac hypertrophy and fibrosis and improves cardiac function in a transgenic rabbit model of human hypertrophic cardiomyopathyR Patel
Section of Cardiology, Department of Medicine, The DeBakey Heart Center, The Methodist Hospital and Baylor College of Medicine, Houston, Texas, USA
Circulation 104:317-24. 2001..These findings highlight the need for clinical trials to determine the effects of simvastatin on cardiac hypertrophy, fibrosis, and dysfunction in humans with hypertrophic cardiomyopathy and heart failure...
- Mutations of the beta myosin heavy chain gene in hypertrophic cardiomyopathy: critical functional sites determine prognosisA Woo
Division of Cardiology, Toronto General Hospital, University Health Network, University of Toronto, Toronto, Ontario, Canada
Heart 89:1179-85. 2003....
- Mutation of Arg723Gly in beta-myosin heavy chain gene in five Chinese families with hypertrophic cardiomyopathyJun Hua Yang
Department of Cardiology, First Affiliated Hospital of Soochow University, Suzhou 215006, China
Chin Med J (Engl) 119:1785-9. 2006..This study was to reveal the disease-causing gene mutations in Chinese population with HCM, and to analyze the correlation between the genotype and phenotype...
- Role of mitogen-activated protein kinase pathway in reactive oxygen species-mediated endothelin-1-induced beta-myosin heavy chain gene expression and cardiomyocyte hypertrophyTzu Hurng Cheng
Department of Medicine, Taipei Medical University Wan Fang Hospital, Taiwan
J Biomed Sci 12:123-33. 2005..These data demonstrate the involvement of ROS in ET-1-induced hypertrophic responses and beta-MyHC expression. ROS mediate ET-1-induced activation of MAPK pathways, which culminates in hypertrophic responses and beta-MyHC expression...
- Role of myocyte-specific enhancer-binding factor (MEF-2) in transcriptional regulation of the alpha-cardiac myosin heavy chain geneE A Adolph
Department of Medicine, University of Cincinnati College of Medicine, Ohio 45267 0575
J Biol Chem 268:5349-52. 1993..In addition, cardiac-specific expression of the transgene was perturbed with significant levels of ectopic expression occurring in the aorta...
- Heavy long-term ethanol consumption induces an alpha- to beta-myosin heavy chain isoform transition in ratJ Meehan
University of Illinois at Chicago, Department of Physiology and Biophysics, 60612, USA
Basic Res Cardiol 94:481-8. 1999..A functional consequence of this transition in MHC phenotype is demonstrated by significant decreases in the myofibrillar and myosin ATPase activities...
- Impact of beta-myosin heavy chain isoform expression on cross-bridge cycling kineticsVeronica L M Rundell
Center for Cardiovascular Research, Department of Physiology and Biophysics, University of Illinois at Chicago, Chicago, Illinois 60612, USA
Am J Physiol Heart Circ Physiol 288:H896-903. 2005..05 (ANOVA)] Thus cross-bridge cycling, under high strain, for alpha-MHC is three times higher than for beta-MHC. Furthermore, under isometric conditions, alpha-MHC and beta-MHC cross bridges hydrolyze ATP independently of one another...
- Diastolic dysfunction without left ventricular hypertrophy is an early finding in children with hypertrophic cardiomyopathy-causing mutations in the beta-myosin heavy chain, alpha-tropomyosin, and myosin-binding protein C genesTuija Poutanen
Department of Pediatrics, Kuopio University Hospital, Kuopio, Finland
Am Heart J 151:725.e1-725.e9. 2006..We investigated the presence of left ventricular hypertrophy (LVH) and features of diastolic dysfunction in genotype-confirmed children from families with hypertrophic cardiomyopathy (HCM) and healthy control children...
- Different phenotypes among slow/beta myosin heavy chain-containing fibres of rabbit masseter muscle: a novel type of diversity in adult muscleA W English
Department of Cell Biology, Emory University School of Medicine, Atlanta, Georgia, USA
J Muscle Res Cell Motil 19:525-35. 1998..We feel that it is a regulated process and that, at least for some phenotypes, this regulation may be hormonally influenced...
- Simultaneous quantification of human cardiac alpha- and beta-myosin heavy chain proteins by MALDI-TOF mass spectrometrySteve M Helmke
Proteomics Facility, Box C 238, University of Colorado Health Sciences Center, 4200 East Ninth Avenue, Denver, Colorado 80262, USA
Anal Chem 76:1683-9. 2004..This method is of general applicability, especially when isoform quantification is required...
- Functional effects of the hypertrophic cardiomyopathy R403Q mutation are different in an alpha- or beta-myosin heavy chain backboneSusan Lowey
Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, VT 05405, USA
J Biol Chem 283:20579-89. 2008..Thus, the functional consequences of the mutation are fundamentally changed depending upon the context of the cardiac MHC isoform...
- Dissociation of left ventricular hypertrophy, beta-myosin heavy chain gene expression, and myosin isoform switch in rats after ascending aortic stenosisR J Wiesner
Department of Physiology, University of Heidelberg, Germany
Circulation 95:1253-9. 1997..In the present investigation, beta-MHC gene expression was studied in an experimental model of pressure-over-load hypertrophy that is not associated with a concurrent activation of the circulating renin-angiotensin system...
- Increased beta-myosin heavy chain in acute cellular rejection following human heart transplantationMohamad H Yamani
Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Kaufman Center for Heart Failure, OH, USA
Am J Transplant 2:386-8. 2002..However, altered expression of beta-myosin heavy chain in human cardiac rejection has not been determined...
- Long-term alcohol administration inhibits synthesis of both myofibrillar and sarcoplasmic proteins in heartThomas C Vary
Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA
Metabolism 54:212-9. 2005..We conclude that translational control mechanisms appear to be important in regulating the expression of myocardial proteins during long-term ethanol intoxication...
- The CAAT-binding transcription factor 1/nuclear factor 1 binding site is important in beta-myosin heavy chain antisense promoter regulation in ratsJulia M Giger
Department of Physiology and Biophysics, University of California, Irvine, D 346, Medical Sciences Building I, Irvine, CA 92697, USA
Exp Physiol 94:1163-73. 2009..Based on these findings, we conclude that the NF1 site is critical to betaAS promoter regulation...
- Human homozygous R403W mutant cardiac myosin presents disproportionate enhancement of mechanical and enzymatic propertiesDagmar I Keller
INSERM U582, Institut de Myologie, , , 47, , 75651 Paris Cedex 13, France
J Mol Cell Cardiol 36:355-62. 2004..Most families present mutations in MYBPC3 and MYH7 encoding cardiac myosin-binding protein C and beta-myosin heavy chain...
- Analysis of myosin heavy chain functionality in the heartMaike Krenz
Cincinnati Children s Hospital Medical Center, The Children s Hospital Research Foundation, MLC 7020, Cincinnati, Ohio 45229 3039, USA
J Biol Chem 278:17466-74. 2003..In mouse cardiac isoforms, myosin functionality does not depend on Loop 1 or Loop 2 sequences and must lie partially in other non-homologous residues...
- Localization of the binding site of the C-terminal domain of cardiac myosin-binding protein-C on the myosin rodEmily Flashman
Department of Cardiovascular Medicine, University of Oxford, Wellcome Trust Centre of Human Genetics, Oxford OX3 7BN, UK
Biochem J 401:97-102. 2007..No effect of these mutations on C10 binding was however detected. We interpret our results with respect to the localization of the proposed trimeric collar on the thick filament...
- A MyoD1-independent muscle-specific enhancer controls the expression of the beta-myosin heavy chain gene in skeletal and cardiac muscle cellsW R Thompson
Howard Hughes Medical Institute, Department of Cardiology, Children s Hospital, Boston, Massachusetts
J Biol Chem 266:22678-88. 1991..These observations provide evidence for the existence of myogenic regulatory programs that precede and/or differ from those governed by known myogenic helix-loop-helix transactivators...
- Effects of cardiac myosin isoform variation on myofilament function and crossbridge kinetics in transgenic rabbitsTakeki Suzuki
Department of Medicine, Cardiology Unit, Fletcher Allen Health Care, Burlington, VT 05401, USA
Circ Heart Fail 2:334-41. 2009..This study was undertaken to identify a myofilament-based mechanism underlying tachycardia-induced cardiomyopathy protection and to extrapolate the impact of MHC isoform variation on myofilament function in human hearts...
- Myopathies associated with myosin heavy chain mutationsA Oldfors
Department of Pathology, Sahlgrenska University Hospital, Goteborg, Sweden
Acta Myol 23:90-6. 2004..Three major MyHC isoforms are expressed in human skeletal muscle (type I, MYH7, expressed in type 1 fibres; IIa, MYH2, expressed in 2A fibres; IIx, MYH1, expressed in 2B fibres)...
- Investigation of a truncated cardiac troponin T that causes familial hypertrophic cardiomyopathy: Ca(2+) regulatory properties of reconstituted thin filaments depend on the ratio of mutant to wild-type proteinC Redwood
Department of Cardiovascular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK
Circ Res 86:1146-52. 2000..Further, these findings underscore the importance of studying mixed mutant:wild-type preparations to faithfully model this autosomal-dominant disease...
- Tissue Doppler imaging consistently detects myocardial contraction and relaxation abnormalities, irrespective of cardiac hypertrophy, in a transgenic rabbit model of human hypertrophic cardiomyopathyS F Nagueh
Section of Cardiology, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA
Circulation 102:1346-50. 2000....
- Enhanced transmural fiber rotation and connexin 43 heterogeneity are associated with an increased upper limit of vulnerability in a transgenic rabbit model of human hypertrophic cardiomyopathyCrystal M Ripplinger
Department of Biomedical Engineering, Washington University, St Louis, MO 63130, USA
Circ Res 101:1049-57. 2007....
- [Genetic causes of hypertrophic cardiomyopathy]H P Vosberg
Max Planck Institut fur Physiologische und Klinische Forschung, Abteilung Experimentelle Kardiologie, Bad Nauheim
Med Klin (Munich) 93:252-9. 1998....
- Clinical features and outcome of hypertrophic cardiomyopathy associated with triple sarcomere protein gene mutationsFrancesca Girolami
Unit for Genetic Diagnosis, Careggi University Hospital, Florence, Italy
J Am Coll Cardiol 55:1444-53. 2010..The aim of this study was to describe the clinical profile associated with triple sarcomere gene mutations in a large hypertrophic cardiomyopathy (HCM) cohort...
- The molecular genetic basis for hypertrophic cardiomyopathyA J Marian
Section of Cardiology, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA
J Mol Cell Cardiol 33:655-70. 2001..Understanding the pathogenesis of HCM could provide for genetic based diagnosis, risk stratification, treatment and prevention of cardiac phenotypes...
- Subclinical skeletal muscle abnormalities in patients with hypertrophic cardiomyopathy and their relation to clinical characteristicsAris Anastasakis
Department of Cardiology, University of Athens, Hippokration Hospital, Athens, Greece
Int J Cardiol 89:249-56. 2003....
- Cocaine produces cardiac hypertrophy by protein kinase C dependent mechanismsRobert J Henning
Department of Medicine, University of South Florida College of Medicine and the James A Haley Hospital, Tampa, Florida, USA
J Cardiovasc Pharmacol Ther 8:149-60. 2003..We determined whether cocaine directly increases cardiomyocyte protein content and whether protein kinase C is important in this process...
- Atrial natriuretic factor and brain natriuretic peptide gene expression in the spontaneous hypertensive rat during postnatal developmentM L Kuroski de Bold
Department of Pathology, University of Ottawa Heart Institute, Ottawa Civic Hospital, ON, Canada
Am J Hypertens 11:1006-18. 1998..The regulation of NP is not coordinated in either gender during the development of hypertension. The activation of the BNP gene in female SHR suggests that BNP might play an important role at the onset of hypertension...
- Altered cardiac hormone and contractile protein messenger RNA levels following left ventricular myocardial infarction in the rat: an in situ hybridization histochemical studyR L Young
University of Melbourne, Department of Medicine, Austin, Australia
Cardiovasc Res 37:187-201. 1998..The present study examined the spatiotemporal expression of cardiac contractile protein and peptide hormone mRNA following left ventricular myocardial infarction (LVMI) in the rat heart...
- Cocaine activates calcium/calmodulin kinase II and causes cardiomyocyte hypertrophyRobert J Henning
Department of Medicine, University of South Florida College of Medicine and the James A Haley VA Hospital, Tampa, Florida 33612, USA
J Cardiovasc Pharmacol 48:802-13. 2006..6%, and beta-MHC by 66.2% (P < 0.01) and significantly decreased cocaine-induced Ca transients and [Ca]i. We conclude that CaMKII activation is an important mechanism whereby cocaine can cause myocyte hypertrophy...
- [Genetics of dilated cardiomyopathy]K J Osterziel
Franz Volhard Klinik Charité Humboldt Universität zu Berlin 13122 Berlin, Germany
Z Kardiol 90:461-9. 2001..Better understanding of the expression and function of disease genes may eventually result in new diagnostic and therapeutic tools in order to improve the prognosis of this severe disorder...
- [Genetics of hereditary cardiopathies]S Debrus
CRBM, CNRS UPR 9008 et INSERM U249, Montpellier
Arch Mal Coeur Vaiss 89:619-27. 1996..1, 3p22 and 12q1). In the near future, these incoming data will deeply modify the cardiovascular field...
- Combined effects of ramipril and angiotensin II receptor blocker TCV116 on rat congestive heart failure after myocardial infarctionZe wei Tao
Department of Cardiology, Chinese People Armed Police Force Hospital of Hunan Province, Changsha 410006, China
Chin Med J (Engl) 118:146-54. 2005..The present study was conducted to examine the combined effects of a chronic ACEI, ramipril, and a chronic Ang II type 1 receptor blocker, TCV116, on rat CHF after myocardial infarction (MI)...
- Insights into human beta-cardiac myosin function from single molecule and single cell studiesSivaraj Sivaramakrishnan
Department of Biochemistry, Stanford University, Stanford, CA, USA
J Cardiovasc Transl Res 2:426-40. 2009..Thirty percent of the point mutations that result in hypertrophic cardiomyopathy are localized to MYH7, the gene encoding human beta-cardiac myosin heavy chain (beta-MyHC)...
- Increased protein kinase C activity in myotrophin-induced myocyte growthP Sil
Department of Molecular Cardiology, The Lerner Research Institute, The Cleveland Clinic Foundation, Ohio 44195, USA
Circ Res 82:1173-88. 1998..Our data suggest that myotrophin exerts its action on protein synthesis, possibly through a tyrosine kinase-coupled pathway and translocation of PKC from the cytosol to the cell membrane...
- Novel cell lines derived from adult human ventricular cardiomyocytesMercy M Davidson
Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
J Mol Cell Cardiol 39:133-47. 2005..These cell lines are potentially useful in vitro models to study developmental regulation of cardiomyocytes in normal and pathological states...
- [Clinical features of dilated cardiomyopathy-like hypertrophic cardiomyopathy caused by a 13261 G > A mutation in cardiac myosin-binding protein C gene]Shu xia Wang
Sino German Laboratory for Molecular Medicine, Fu Wai Cardiovascular Hospital and Cardiovascular Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China
Zhonghua Xin Xue Guan Bing Za Zhi 35:17-20. 2007..To study the disease-causing gene mutation in Chinese patients with hypertrophic cardiomyopathy (HCM) and to analyze the genotype and phenotype correlation...
- Expression of proto-oncogenes and gene mutation of sarcomeric proteins in patients with hypertrophic cardiomyopathyH Kai
From the Cardiovascular Research Institute, Kurume University and the Third Department of Internal Medicine, Kurume University School of Medicine, Kurume, Japan
Circ Res 83:594-601. 1998..It is possible that ss-MHC gene mutation has some effect on the regulation of proto-oncogene expression in HCM...
- Evidence of MyomiR network regulation of beta-myosin heavy chain gene expression during skeletal muscle atrophyJohn J McCarthy
Department of Physiology, College Health Sciences, University of Kentucky, Lexington, Kentucky 40536 0298, USA
Physiol Genomics 39:219-26. 2009..These results further expand the role of miRs in adult skeletal muscle and are consistent with a model in which the MyomiR network regulates slow myosin expression during muscle atrophy...
- Reduced inotropic reserve and increased susceptibility to cardiac ischemia/reperfusion injury in phosphocreatine-deficient guanidinoacetate-N-methyltransferase-knockout miceMichiel Ten Hove
Department of Cardiovascular Medicine, University of Oxford, Oxford, England
Circulation 111:2477-85. 2005..To characterize the role of a substantially impaired CK/PCr system in heart, we studied the cardiac phenotype of wild-type (WT) and GAMT-/- mice...
- Gender differences in molecular remodeling in pressure overload hypertrophyE O Weinberg
Charles A Dana Research Institute, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
J Am Coll Cardiol 34:264-73. 1999..The objective of this study was to examine gender differences in left ventricular (LV) function and expression of cardiac genes in response to LV pressure overload due to ascending aortic stenosis in rats...
- The antioxidant tempol inhibits cardiac hypertrophy in the insulin-resistant GLUT4-deficient mouse in vivoR H Ritchie
Molecular Pharmacology Laboratory, Wynn Department of Metabolic Cardiology, Baker Heart Research Institute, St Kilda Road Central, Melbourne, VIC 8008, Australia
J Mol Cell Cardiol 42:1119-28. 2007..Antioxidants may offer new alternatives in this disorder...
- Rescuing the N-cadherin knockout by cardiac-specific expression of N- or E-cadherinY Luo
Center for Research on Reproduction and Women s Health, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Development 128:459-69. 2001....
- Progressive atrioventricular conduction defects and heart failure in mice expressing a mutant Csx/Nkx2.5 homeoproteinH Kasahara
Cardiovascular Division, Beth Israel Deaconess Medical Center, and Department of Medicine, Children s Hospital, Boston, Massachusetts, USA
J Clin Invest 108:189-201. 2001..This transgenic mouse model may be useful in the study of the pathogenesis of cardiac dysfunction associated with CSX/NKX2.5 mutations in humans...
- Ral GDP dissociation stimulator and Ral GTPase are involved in myocardial hypertrophyMiki Kawai
Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, 7 5 2, Kusunoki cho, Chuo Ku, Kobe 650 0017, Japan
Hypertension 41:956-62. 2003..SATA3 may play a key role in Ral-GDS expression and Ral activation. Our data provide evidence that the Ral-GDS/Ral signaling pathway is a link to the process of cardiac hypertrophy...
- Mutations profile in Chinese patients with hypertrophic cardiomyopathyLei Song
Sino German Laboratory for Molecular Medicine, Fuwai Hospital and Cardiovascular Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China
Clin Chim Acta 351:209-16. 2005..There are more than 1 million patients with hypertrophic cardiomyopathy (HCM) in China, but the genetic basis is presently unknown...
- How accurately do semi-permeable membrane devices measure the bioavailability of polycyclic aromatic hydrocarbons to Daphnia magna?Catherine Gourlay
Cemagref, Unité de Recherches Hydrosystèmes et Bioprocédés, Parc de Tourvoie, BP 44, 92163 Antony cedex, France
Chemosphere 61:1734-9. 2005..This study aims at evaluating the ability for SPMD to sample polycyclic aromatic hydrocarbons (fluoranthene, pyrene and benzo[a]pyrene) that are actually bioavailable ..
- Comparison of mussels and semi-permeable membrane devices as intertidal monitors of polycyclic aromatic hydrocarbons at oil spill sitesPaul D Boehm
Exponent, 2 Clock Tower Place, Suite 340, Maynard, MA 01754, USA
Mar Pollut Bull 50:740-50. 2005..and mussels collected adjacent to those pits at oiled sites were higher than in SPMDs and mussels from non-pitted SPMD locations approximately 3-15 m from the pits. Pitting released buried oil making its PAH bioavailable...
- Prevention of cardiac hypertrophy by atorvastatin in a transgenic rabbit model of human hypertrophic cardiomyopathyVinitha Senthil
Department of Medicine, Baylor College of Medicine, One Baylor Plaza, 519D, Houston, TX 77030, USA
Circ Res 97:285-92. 2005..The results indicate potential beneficial effects of atorvastatin in prevention of cardiac hypertrophy, a major determinant of morbidity in all forms of cardiovascular diseases, and beckon clinical studies in humans with HCM...
- In vitro cardiomyogenic differentiation of adult human bone marrow mesenchymal stem cells. The role of 5-azacytidinePolychronis Antonitsis
First Department of Thoracic and Cardiovascular Surgery, Aristotle University of Thessaloniki, AHEPA Hospital, Thessaloniki, Greece
Interact Cardiovasc Thorac Surg 6:593-7. 2007..These results indicate that adult human bone marrow mesenchymal stem cells can differentiate towards a cardiomyogenic lineage in vitro...
- Structural effects of the slow/b-cardiac myosin heavy chain R453C mutation in cardiac and skeletal muscleHoma Tajsharghi
Department of Pathology, Sahlgrenska University Hospital, Goteborg, Sweden
Scand Cardiovasc J 42:153-6. 2008..In some families, HCM is caused by distinct mutations of the cardiac beta myosin heavy chain gene (MYH7).
- Hypertrophic cardiomyopathy due to beta-myosin heavy chain mutation with extreme phenotypic variability within a familyD I Keller
Department of Cardiology, University Hospital Basel, Switzerland
Int J Cardiol 134:e87-93. 2009..In this case report a family with proven beta-myosin heavy chain mutation (MYH7) with 3 affected family members with huge phenotypic variability is described...
- A de novo mutation of the beta cardiac myosin heavy chain gene in an infantile restrictive cardiomyopathySimon Karam
Department of Pediatric Cardiology, Groupe Hospitalier Est, Hospices Civils de Lyon, Lyon, France
Congenit Heart Dis 3:138-43. 2008..pediatric case of restrictive cardiomyopathy secondary to a de novo mutation in the cardiac myosin heavy chain gene MYH7. The clinical course is characterized by an early onset of disease, mild hypertrophy of the left ventricle and a ..
- The familial hypertrophic cardiomyopathy-associated myosin mutation R403Q accelerates tension generation and relaxation of human cardiac myofibrilsAlexandra Belus
Department of Physiology, University of Florence, Florence, Italy
J Physiol 586:3639-44. 2008..Increased energy cost of tension generation may be central to the FHC disease process, help explain some unresolved clinical observations, and carry significant therapeutic implications...
- Genetic and clinical profile of Indian patients of idiopathic restrictive cardiomyopathy with and without hypertrophyTaranjit Singh Rai
Department of Experimental Medicine and Biotechnology, Post Graduate Institute of Medical Education and Research, Chandigarh, India
Mol Cell Biochem 331:187-92. 2009..We studied a group of patients with restrictive physiology for mutations in beta-myosin heavy chain (MYH7) and troponin I (TNNI3) gene...
- Partitioning of fluorotelomer alcohols (FTOH) to semipermeable membrane devices (SPMD)Stefan Fiedler
Helmholtz Zentrum Munchen, National Research Centre for Environmental Health, Institute of Ecological Chemistry, Ingolstaedter Landstrasse 1, 85764, Neuherberg, Germany
Environ Sci Pollut Res Int 17:420-8. 2010..In this study, triolein-filled low-density polyethylene tubes were used as semipermeable membrane devices (SPMD) and tested for their suitability as passive air samplers for FTOH.
- Exogenous expression of HIF-1 alpha promotes cardiac differentiation of embryonic stem cellsKwong Man Ng
Stem Cell and Regenerative Medicine Program, Research Centre of Heart, Brain, Hormone and Healthy Ageing, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China
J Mol Cell Cardiol 48:1129-37. 2010..These findings suggest that keen activation of the HIF-1 pathway enhances differentiation and maturation of cardiomyocytes derived from ESCs...
- Peripheral benzodiazepine receptor ligand Ro5-4864 inhibits isoprenaline-induced cardiac hypertrophy in ratsAmardeep Jaiswal
Department of Pharmacology, All India Institute of Medical Sciences, New Delhi 110029, India
Eur J Pharmacol 644:146-53. 2010..This is the first study to demonstrate a salutary effect of Ro5-4864 in experimental cardiac hypertrophy...
- Prevalence and spectrum of mutations in a cohort of 192 unrelated patients with hypertrophic cardiomyopathyGilles Millat
Laboratoire de Cardiogénétique Moléculaire, Centre de biologie et pathologie est, Hospices Civils de Lyon, Lyon, France
Eur J Med Genet 53:261-7. 2010..unrelated HCM patients using denaturing high-performance liquid chromatography/sequencing analysis of the MYBPC3, MYH7, TNNT2 and TNNI3 genes...
- Novel mutation in MYH7 gene associated with distal myopathy and cardiomyopathyHouman Homayoun
Department of Neurology, University of Pittsburgh, Pittsburgh, PA 15213, USA
Neuromuscul Disord 21:219-22. 2011..We identified a de-novo, heterozygous, missense mutation, c.2348G>C (p. Arg783Pro), in exon 21 of the MYH7 gene, which encodes slow skeletal muscle fiber/β-cardiac myosin heavy chain protein, that replaces a highly ..
- Cardiovascular effects of chronic treatment with a β2-adrenoceptor agonist relieving neuropathic pain in miceNada Choucair-Jaafar
Institut des Neurosciences Cellulaires et Integratives, Centre National de la Recherche Scientifique, 21 rue René Descartes, 67084 Strasbourg Cedex, France
Neuropharmacology 61:51-60. 2011..natriuretic peptide (Nppa), periostin (Postn), connective tissue growth factor (Ctgf) and β-myosin heavy chain (Myh7)...
- Developmental expression and cardiac transcriptional regulation of Myh7b, a third myosin heavy chain in the vertebrate heartAndrew S Warkman
Department of Cellular and Molecular Medicine, University of Arizona Health Sciences Center, Tucson, Arizona 85724, USA
Cytoskeleton (Hoboken) 69:324-35. 2012The mammalian heart expresses two myosin heavy chain (MYH) genes (Myh6 and Myh7), which are major components of the thick filaments of the sarcomere. We have determined that a third MYH, MYH7B, is also expressed in the myocardium...
- A novel mutation expands the genetic and clinical spectrum of MYH7-related myopathiesNigel F Clarke
INMR, The Children s Hospital at Westmead and Discipline of Paediatrics and Child Health, University of Sydney, Sydney, Australia
Neuromuscul Disord 23:432-6. 2013b>MYH7 mutations are an established cause of Laing distal myopathy, myosin storage myopathy, and cardiomyopathy, as well as additional myopathy subtypes. We report a novel MYH7 mutation (p...
- Novel mutations widen the phenotypic spectrum of slow skeletal/β-cardiac myosin (MYH7) distal myopathyPhillipa J Lamont
Neurogenetic Unit, Department of Neurology, Royal Perth Hospital, Western Australia, Australia Diagnostic Genomics Laboratory, PathWest, Queen Elizabeth II Medical Centre, Nedlands, Western Australia, Australia
Hum Mutat 35:868-79. 2014..myosin storage myopathy are caused by mutations of slow skeletal/β-cardiac myosin heavy chain encoded by the gene MYH7, as is a common form of familial hypertrophic/dilated cardiomyopathy...
- MOTOR FUNCTION OF CARDIAC B MYOSIN MUTANTSMitsuo Ikebe; Fiscal Year: 1999....
- ACTIVITY & METABOLIC CONTROL OF CARDIAC B MYOSINKENNETH BALDWIN; Fiscal Year: 2001..These approaches will collectively delineate the molecular mechanisms responsible for the regulation of beta MHC expression in the in vivo setting. ..
- DEVELOPMENTAL AGE AND CHANGES IN MYOSIN ISOZYMESFrank Stockdale; Fiscal Year: 1999..The aim of these experiments is to determine the biological basis for innervation-dependent differentiation and identify the elements of the slow MyHC 3 gene responsive in selective activation of slow MyHC 3 by innervation. ..
- Molecular Epidemiology of Dilated CardiomyopathLuisa Mestroni; Fiscal Year: 2005..abstract_text> ..
- SIGNALS OF OXIDANT INDUCED CARDIOMYOCYTE HYPERTROPHYQin Chen; Fiscal Year: 1999..We propose to study the mechanism of oxidant stress by novel and innovative approaches. The results will contribute to the understanding of the process of heart aging and the pathogenesis of heart failure. ..
- PTH RELATED PROTEIN IN VASCULAR SMOOTH MUSCLEThomas Clemens; Fiscal Year: 2004..We will determine the consequence of cardiac-specific ablation of PTHrP and its receptor on heart development by crossing a beta-myosin heavy chain driven Cre mouse with the PTHrP and PTHrP and PTHrP-R floxed mice. ..
- MECHANICAL REGULATION OF CARDIAC METABOLISMDavid Simpson; Fiscal Year: 2000....
- Genetic and Molecular Signaling in Heart FailureEvangelia Kranias; Fiscal Year: 2009..We believe this thematically linked, multidisciplinary Center will continue to break new ground in understanding the pathogenesis and optimal management of heart failure. ..
- Wen Yi Chen; Fiscal Year: 2014..Of these, more than 80% can be found in 7 genes, namely LMNA, MYH6, MYH7, MYPN, TNNT2, SCN5a, and MYBPC3...
- MANNITOL AND VIRULENCE IN CRYPTOCOCCUS NEOFORMANSBrian Wong; Fiscal Year: 2002..Therefore, he will (i) clone and sequence the C. neoformans MPD structural gene (MPD1), (ii) construct mpd1 null mutants, and (iii) test these mutants for their abilities to synthesize and catabolize ..
- Multidisciplinary Study of Right Ventricular DysplasiaJeffrey Towbin; Fiscal Year: 2005..This integrated research grant proposal offers a substantial prospect of expanding the fund of clinical knowledge regarding ARVD and of localizing the gene(s) responsible for this disorder. ..
- ALTERED MECHANICAL LOADS AND SKELETAL MUSCLE PHENOTYPERichard Tsika; Fiscal Year: 2009..abstract_text> ..
- EXERCISE HYPERTROPHY AND CONTROL OF MYOSIN INDUCTIONRichard Tsika; Fiscal Year: 2008..abstract_text> ..
- Structure and Function of Myosin VIHUGH SWEENEY; Fiscal Year: 2006..determine which kinetic and structural features are necessary for processive movement and the large step size of myosin VI; and 3) delineate putative modes of regulation of the myosin VI motor. ..
- Inherited myosin mutations that cause heart diseaseTodd Herron; Fiscal Year: 2006..unreadable] [unreadable]..
- Cardiac Hypertrophy Due to Oxidative Stress InsulinThunder Jalili; Fiscal Year: 2006..unreadable] [unreadable] [unreadable]..
- Steroid As Cytoprotectants against Oxidative ToxicityQin Chen; Fiscal Year: 2007..unreadable] [unreadable] [unreadable]..
- Alcohol-Induced Regulation of Hepatic Protein SynthesisTHOMAS VARY; Fiscal Year: 2007..unreadable] [unreadable] [unreadable]..
- Understanding and Preventing Disuse AtrophyHUGH SWEENEY; Fiscal Year: 2007..abstract_text> ..
- Proteoglycan degradation and functional recovery after peripheral nerve injuryARTHUR ENGLISH; Fiscal Year: 2007..This proposal seeks to evaluate a technology for medical treatment of peripheral nerve injuries which, if successful, could have an important impact on a relatively large group of under-treated patients. [unreadable] [unreadable]..
- Role of Acetaldehyde in Alcoholic CardiomyopathyJun Ren; Fiscal Year: 2008..Our long-term goal is to establish the toxic mechanism of acetaldehyde in the development of alcoholic cardiomyopathy so that prevention and treatment can be optimized [unreadable] [unreadable]..
- IN VIVO STUDIES OF TROPONIN T FUNCTIONHUGH SWEENEY; Fiscal Year: 2002..Our findings will provide fundamental knowledge of the mechanisms of muscle contraction and a basis for development of gene and drug therapies for the treatment of HCM. ..
- Mechanisms of myopathy caused by mutations in the myosin rodLESLIE ANNE LEINWAND; Fiscal Year: 2010..Relevance to public health: Genetic heart disease is an important health problem and this specific type of heart disease we study is the leading cause of sudden death in young people. ..
- Translational Control of Oxidative Stress in Myocardial InfarctionQin M Chen; Fiscal Year: 2010..PUBLIC HEALTH RELEVANCE: This grant proposes to study the mechanism of Nrf2 protein translation in cardiomyocytes and in the myocardium following oxidative stress. ..
- MYOSIN ISOZYMESHUGH LEE SWEENEY; Fiscal Year: 2010....
- Conference on Molecular Biology of the HeartLeslie Leinwand; Fiscal Year: 2002..It will be a multidisciplinary meeting that should bring together people who are beginning to have regular dialogues but whose traditions have been somewhat separate. ..
- Developmental Myosin Heavy Chain Regulation and FunctionLeslie Leinwand; Fiscal Year: 2006..Specifically, we will test the hypothesis that embryonic MyHC contractile function is necessary for muscle development. These studies will define the role of the developmental MyHC isoforms in skeletal muscle form and function. ..
- Cross Talk in Retinoid Teratology in Neural CrestMelissa Colbert; Fiscal Year: 2003....
- Muscle: Contractile Proteins GRC 2005HUGH SWEENEY; Fiscal Year: 2005..This will be a transitional conference in that the overall focus of the conference will be divided between the Molecular Basis of Muscle Contraction and the broader topic of the Design and Function of Molecular Motors. ..
- Hereditary spastic paraplegia linked to chromosomes 8qPeter Hedera; Fiscal Year: 2006..I will characterize the phenotype of transgenic animals. The study of a transgenic animal model will further enhance current state of knowledge about the pathophysiology of HSP and axonal degeneration. ..
- Zic3 and the Control of Body Pattern FormationSTEPHANIE WARE; Fiscal Year: 2005..Through a combination of supervised research, scientific interchange, and selected coursework within this environment, the candidate will obtain the training necessary to transition to an independent investigator. ..
- Proteome Mapping of Heart Failure in AgingMARVIN BOLUYT; Fiscal Year: 2005..Identification of proteins involved in aldosterone signaling will lead to the development of new hypotheses for future grant proposals addressing their roles in the development of heart failure in the elderly. ..
- MECHANISMS OF CARDIOVASCULAR DISEASE AND GENE THERAPYLeslie Leinwand; Fiscal Year: 2005..In addition, we have established a formal link with the MD-PhD) program in Denver that allows those students to do their thesis work in Boulder. This training grant can facilitate those ventures. ..
- BIOENGINEERING RESEARCH PARTNERSHIP--MUSCULAR DYSTROPHYHUGH SWEENEY; Fiscal Year: 2004..Lee Sweeney, Ph.D.); and Section 3: development of non-invasive methods for monitoring therapeutic benefits of dystrophin gene transfer (directed by Glenn Walter, Ph.D.). ..
- DENVER CARDIOVASCULAR HEALTH EDUCATION ALLIANCE, PHASE ILeslie Leinwand; Fiscal Year: 2004..abstract_text> ..
- MOLECULAR MECHANISMS OF OXIDANT TOXICITYQin Chen; Fiscal Year: 2004..We have a unique finding of premature senescence with oxidative stress and will combine in vitro and in vivo approaches to uncover the trigger of unwanted effects of aging. ..
- REGULATION OF MASTICATORY MUSCLE FIBER PHENOTYPEARTHUR ENGLISH; Fiscal Year: 2002..The new knowledge generated will impact significantly several areas of clinical dentistry. ..
- IGF-1, Oxidative Stress and Cardiovascular AgingJun Ren; Fiscal Year: 2002..Our long-term goal is to establish the causal link among IGF-1 deficiency, enhanced oxidative damage and ventricular dysfunction in the progression of cardiovascular aging so that hormonal or antioxidant therapy can be optimized...
- TRAINING IN MUSCLE BIOLOGYHUGH SWEENEY; Fiscal Year: 2003..This is evidenced by the many prominent scientists around the world, who have trained in this field at the University of Pennsylvania. ..