Genomes and Genes
Gene Symbol: Myh7
Description: myosin, heavy polypeptide 7, cardiac muscle, beta
Alias: B-MHC, MYH-beta/slow, MyHC-I, Myhc-b, Myhcb, beta-MHC, betaMHC, myHC-beta, myHC-slow, myosin-7, myosin heavy chain 7, myosin heavy chain slow isoform, myosin heavy chain, cardiac muscle beta isoform, myosin heavy chain, cardiac muscle, fetal
- Maitra M, Schluterman M, Nichols H, Richardson J, Lo C, Srivastava D, et al. Interaction of Gata4 and Gata6 with Tbx5 is critical for normal cardiac development. Dev Biol. 2009;326:368-77 pubmed publisher..These findings highlight the unique genetic interactions of Gata4 and Gata6 with Tbx5 for normal cardiac morphogenesis in vivo. ..
- Delgado Olguin P, Huang Y, Li X, Christodoulou D, Seidman C, Seidman J, et al. Epigenetic repression of cardiac progenitor gene expression by Ezh2 is required for postnatal cardiac homeostasis. Nat Genet. 2012;44:343-7 pubmed publisher..Our results suggest that epigenetic dysregulation in embryonic progenitor cells is a predisposing factor for adult disease and dysregulated stress responses. ..
- Lyons I, Parsons L, Hartley L, Li R, Andrews J, Robb L, et al. Myogenic and morphogenetic defects in the heart tubes of murine embryos lacking the homeo box gene Nkx2-5. Genes Dev. 1995;9:1654-66 pubmed..The data demonstrate that Nkx2-5 is essential for normal heart morphogenesis, myogenesis, and function. Furthermore, this gene is a component of a genetic pathway required for myogenic specialization of the ventricles. ..
- Misra C, Sachan N, McNally C, Koenig S, Nichols H, Guggilam A, et al. Congenital heart disease-causing Gata4 mutation displays functional deficits in vivo. PLoS Genet. 2012;8:e1002690 pubmed publisher..In summary, the Gata4 G295S mutation functions as a hypomorph in vivo and leads to defects in cardiomyocyte proliferation during embryogenesis, which may contribute to the development of congenital heart defects in humans. ..
- Thackaberry E, Bedrick E, Goens M, Danielson L, Lund A, Gabaldon D, et al. Insulin regulation in AhR-null mice: embryonic cardiac enlargement, neonatal macrosomia, and altered insulin regulation and response in pregnant and aging AhR-null females. Toxicol Sci. 2003;76:407-17 pubmed..While the ultimate cause of the neonatal phenotype remains unclear, these studies establish that the AhR is required for normal insulin regulation in pregnant and older mice and for cardiac development in embryonic mice. ..
- LU J, Izvolsky K, Qian J, Cardoso W. Identification of FGF10 targets in the embryonic lung epithelium during bud morphogenesis. J Biol Chem. 2005;280:4834-41 pubmed..Our approach identifies Fgf10 targets that are common to multiple biological processes and provides insights into potential mechanisms by which Fgf signaling regulates epithelial cell behavior. ..
- Anderson D, Anderson K, Chang C, Makarewich C, Nelson B, McAnally J, et al. A micropeptide encoded by a putative long noncoding RNA regulates muscle performance. Cell. 2015;160:595-606 pubmed publisher..These findings identify MLN as an important regulator of skeletal muscle physiology and highlight the possibility that additional micropeptides are encoded in the many RNAs currently annotated as noncoding. ..
- Nishi H, Ono K, Horie T, Nagao K, Kinoshita M, Kuwabara Y, et al. MicroRNA-27a regulates beta cardiac myosin heavy chain gene expression by targeting thyroid hormone receptor beta1 in neonatal rat ventricular myocytes. Mol Cell Biol. 2011;31:744-55 pubmed publisher..These findings suggested that miR-27a regulates ?-MHC gene expression by targeting TR?1 in cardiomyocytes. ..
- Oh M, Rybkin I, Copeland V, Czubryt M, Shelton J, van Rooij E, et al. Calcineurin is necessary for the maintenance but not embryonic development of slow muscle fibers. Mol Cell Biol. 2005;25:6629-38 pubmed..These results demonstrate that developmental patterning of slow fibers is independent of calcineurin, while the maintenance of the slow-fiber phenotype in the adult requires calcineurin activity...
- Lu B, Allen D, Leinwand L, Lyons G. Spatial and temporal changes in myosin heavy chain gene expression in skeletal muscle development. Dev Biol. 1999;216:312-26 pubmed..The changes in MyHC RNA and protein expression are distinct in different muscles and are restricted in some cases to particular regions of the muscle and do not always reflect their distribution in the adult. ..
- Grifone R, Jarry T, Dandonneau M, Grenier J, Duprez D, Kelly R. Properties of branchiomeric and somite-derived muscle development in Tbx1 mutant embryos. Dev Dyn. 2008;237:3071-8 pubmed publisher..The critical requirement for Tbx1 during muscle development is thus in the robust onset of myogenic specification in pharyngeal mesoderm. ..
- Sassoon D, Lyons G, Wright W, Lin V, Lassar A, Weintraub H, et al. Expression of two myogenic regulatory factors myogenin and MyoD1 during mouse embryogenesis. Nature. 1989;341:303-7 pubmed
- Uren D, Hwang H, Hara Y, Takeda K, Kawamoto S, Tullio A, et al. Gene dosage affects the cardiac and brain phenotype in nonmuscle myosin II-B-depleted mice. J Clin Invest. 2000;105:663-71 pubmed..These data on B(DeltaI)/B(DeltaI) and B(DeltaI)/B(-) mice demonstrate a gene dosage effect of the amount of NMHC-B on the severity and time of onset of the defects in the heart and brain. ..
- Han P, Li W, Lin C, Yang J, Shang C, Nuernberg S, et al. A long noncoding RNA protects the heart from pathological hypertrophy. Nature. 2014;514:102-106 pubmed publisher..An estimated 70% of mouse genes undergo antisense transcription, including myosin heavy chain 7 (Myh7), which encodes molecular motor proteins for heart contraction...
- Krenz M, Sadayappan S, Osinska H, Henry J, Beck S, Warshaw D, et al. Distribution and structure-function relationship of myosin heavy chain isoforms in the adult mouse heart. J Biol Chem. 2007;282:24057-64 pubmed
- Komatsu Y, Shibuya H, Takeda N, Ninomiya Tsuji J, Yasui T, Miyado K, et al. Targeted disruption of the Tab1 gene causes embryonic lethality and defects in cardiovascular and lung morphogenesis. Mech Dev. 2002;119:239-49 pubmed..These results indicate a possibility that TAB1 plays an important role in mammalian embryogenesis and is required for TAK1 activation in TGF-beta signaling. ..
- Tsika R, Ma L, Kehat I, Schramm C, Simmer G, Morgan B, et al. TEAD-1 overexpression in the mouse heart promotes an age-dependent heart dysfunction. J Biol Chem. 2010;285:13721-35 pubmed publisher..These data provide the first in vivo evidence that increased TEAD-1 can induce characteristics of cardiac remodeling associated with cardiomyopathy and heart failure. ..
- Fassler R, Rohwedel J, Maltsev V, Bloch W, Lentini S, Guan K, et al. Differentiation and integrity of cardiac muscle cells are impaired in the absence of beta 1 integrin. J Cell Sci. 1996;109 ( Pt 13):2989-99 pubmed..Thus, we conclude that interactions with the extracellular matrix via beta 1 integrin is necessary for differentiation and the maintenance of a specialized phenotype of cardiac muscle cells. ..
- Lowey S, Lesko L, Rovner A, Hodges A, White S, Low R, et al. Functional effects of the hypertrophic cardiomyopathy R403Q mutation are different in an alpha- or beta-myosin heavy chain backbone. J Biol Chem. 2008;283:20579-89 pubmed publisher..Thus, the functional consequences of the mutation are fundamentally changed depending upon the context of the cardiac MHC isoform. ..
- Usami A, Abe S, Ide Y. Myosin heavy chain isoforms of the murine masseter muscle during pre- and post-natal development. Anat Histol Embryol. 2003;32:244-8 pubmed..This suggests that the development of murine masseter muscle is closely associated with facial development. ..
- Tian Y, Liu Y, Wang T, Zhou N, Kong J, Chen L, et al. A microRNA-Hippo pathway that promotes cardiomyocyte proliferation and cardiac regeneration in mice. Sci Transl Med. 2015;7:279ra38 pubmed publisher..Our data demonstrate the ability of microRNA-based therapeutic approaches to promote mammalian cardiac repair and regeneration through the transient activation of cardiomyocyte proliferation. ..
- Xu C, Liguori G, Persico M, Adamson E. Abrogation of the Cripto gene in mouse leads to failure of postgastrulation morphogenesis and lack of differentiation of cardiomyocytes. Development. 1999;126:483-94 pubmed..7 embryos: (&agr;)MHC, betaMHC, MLC2A, MLC2V and ANF, whereas they were expressed in wild-type embryos...
- Harrelson Z, Kelly R, Goldin S, Gibson Brown J, Bollag R, Silver L, et al. Tbx2 is essential for patterning the atrioventricular canal and for morphogenesis of the outflow tract during heart development. Development. 2004;131:5041-52 pubmed
- Zammit P, Kelly R, Franco D, Brown N, Moorman A, Buckingham M. Suppression of atrial myosin gene expression occurs independently in the left and right ventricles of the developing mouse heart. Dev Dyn. 2000;217:75-85 pubmed..dev dyn 2000;217:75-85. ..
- Lewandowski S, Janardhan H, Smee K, Bachman M, Sun Z, Lazar M, et al. Histone deacetylase 3 modulates Tbx5 activity to regulate early cardiogenesis. Hum Mol Genet. 2014;23:3801-9 pubmed publisher..These findings reveal that Hdac3 plays a critical role in cardiac progenitor cells to regulate early cardiogenesis. ..
- Tsika R, Schramm C, Simmer G, Fitzsimons D, Moss R, Ji J. Overexpression of TEAD-1 in transgenic mouse striated muscles produces a slower skeletal muscle contractile phenotype. J Biol Chem. 2008;283:36154-67 pubmed publisher..These novel in vivo data support a role for TEAD-1 in modulating slow muscle gene expression. ..
- Fatkin D, Christe M, Aristizabal O, McConnell B, Srinivasan S, Schoen F, et al. Neonatal cardiomyopathy in mice homozygous for the Arg403Gln mutation in the alpha cardiac myosin heavy chain gene. J Clin Invest. 1999;103:147-53 pubmed..We speculate that variable incorporation of mutant and normal MHC into sarcomeres of heterozygotes may account for focal myocyte death in familial hypertrophic cardiomyopathy. ..
- Nakajima K, Inagawa M, Uchida C, Okada K, Tane S, Kojima M, et al. Coordinated regulation of differentiation and proliferation of embryonic cardiomyocytes by a jumonji (Jarid2)-cyclin D1 pathway. Development. 2011;138:1771-82 pubmed publisher..Thus, a Jmj-cyclin D1 pathway coordinately regulates proliferation and differentiation of cardiomyocytes. ..
- Spindler M, Saupe K, Christe M, Sweeney H, Seidman C, Seidman J, et al. Diastolic dysfunction and altered energetics in the alphaMHC403/+ mouse model of familial hypertrophic cardiomyopathy. J Clin Invest. 1998;101:1775-83 pubmed..Changes in high-energy phosphate content suggest that an energy-requiring process may contribute to the observed diastolic dysfunction. ..
- Shin C, Liu Z, Passier R, Zhang C, Wang D, Harris T, et al. Modulation of cardiac growth and development by HOP, an unusual homeodomain protein. Cell. 2002;110:725-35 pubmed..We propose that HOP modulates SRF activity during heart development; its absence results in an imbalance between cardiomyocyte proliferation and differentiation with consequent abnormalities in cardiac morphogenesis. ..
- Xin M, Davis C, Molkentin J, Lien C, Duncan S, Richardson J, et al. A threshold of GATA4 and GATA6 expression is required for cardiovascular development. Proc Natl Acad Sci U S A. 2006;103:11189-94 pubmed
- Jiang C, Wang J, Yue F, Kuang S. The brain expressed x-linked gene 1 (Bex1) regulates myoblast fusion. Dev Biol. 2016;409:16-25 pubmed publisher..These results elucidate a novel role of Bex1 in myogenesis through regulating myoblast fusion. ..
- Kee H, Kim J, Nam K, Park H, Shin S, Kim J, et al. Enhancer of polycomb1, a novel homeodomain only protein-binding partner, induces skeletal muscle differentiation. J Biol Chem. 2007;282:7700-9 pubmed..These results suggest that Epc1 plays a role in the initiation of skeletal muscle differentiation, and its interaction with Hop is required for the full activity. ..
- van Berlo J, Elrod J, van den Hoogenhof M, York A, Aronow B, Duncan S, et al. The transcription factor GATA-6 regulates pathological cardiac hypertrophy. Circ Res. 2010;107:1032-40 pubmed publisher..These results indicate that GATA-6 is both necessary and sufficient for regulating the cardiac hypertrophic response and differentiated gene expression, both alone and in coordination with GATA-4. ..
- Yamaguchi N, Chakraborty A, Pasek D, Molkentin J, Meissner G. Dysfunctional ryanodine receptor and cardiac hypertrophy: role of signaling molecules. Am J Physiol Heart Circ Physiol. 2011;300:H2187-95 pubmed publisher..5 hearts; rather increased Erk1/2 and p90RSK phosphorylation levels likely leading to reduced GSK-3? activity were found to precede development of cardiac hypertrophy in mice expressing dysfunctional ryanodine receptor ion channel. ..
- Petchey L, Risebro C, Vieira J, Roberts T, Bryson J, Greensmith L, et al. Loss of Prox1 in striated muscle causes slow to fast skeletal muscle fiber conversion and dilated cardiomyopathy. Proc Natl Acad Sci U S A. 2014;111:9515-20 pubmed publisher..Our study identifies conserved roles for Prox1 between cardiac and skeletal muscle, specifically implicated in slow-twitch fiber-type specification, function, and cardiomyopathic disease. ..
- Weydert A, Daubas P, Lazaridis I, Barton P, Garner I, Leader D, et al. Genes for skeletal muscle myosin heavy chains are clustered and are not located on the same mouse chromosome as a cardiac myosin heavy chain gene. Proc Natl Acad Sci U S A. 1985;82:7183-7 pubmed..This result is in contrast to that for other contractile protein genes such as the alkali myosin light chain and the actin multigene families, which are dispersed in the genome. ..
- Lee Y, Song A, Baker R, Micales B, Conway S, Lyons G. Jumonji, a nuclear protein that is necessary for normal heart development. Circ Res. 2000;86:932-8 pubmed..These data demonstrate that JMJ is a nuclear protein, which is essential for normal heart development and function. ..
- Gopalakrishnan S, Comai G, Sambasivan R, Francou A, Kelly R, Tajbakhsh S. A Cranial Mesoderm Origin for Esophagus Striated Muscles. Dev Cell. 2015;34:694-704 pubmed publisher..These findings have important implications in understanding esophageal dysfunctions, including dysphagia, and congenital disorders, such as DiGeorge syndrome. ..
- Singh R, Horsthuis T, Farin H, Grieskamp T, Norden J, Petry M, et al. Tbx20 interacts with smads to confine tbx2 expression to the atrioventricular canal. Circ Res. 2009;105:442-52 pubmed publisher..Our data suggest that Tbx20 directly interferes with Bmp/Smad signaling to suppress Tbx2 expression in the chambers, thereby confining Tbx2 expression to the prospective AVC region. ..
- Qi Y, Zhu Q, Zhang K, THOMAS C, Wu Y, Kumar R, et al. Activation of Foxo1 by insulin resistance promotes cardiac dysfunction and Î²-myosin heavy chain gene expression. Circ Heart Fail. 2015;8:198-208 pubmed publisher..Targeting Foxo1 and its regulation will provide novel strategies in preventing metabolic and myocardial dysfunction and influencing MHC plasticity in diabetes mellitus. ..
- Ford S, Chandra M. Length-dependent effects on cardiac contractile dynamics are different in cardiac muscle containing ?- or ?-myosin heavy chain. Arch Biochem Biophys. 2013;535:3-13 pubmed publisher..These data suggest a mechanism whereby greater cooperative/allosteric effects impart an enhanced length-sensitivity of XB cycling kinetics in fibers containing the slower cycling ?-MHC...
- Sigoillot S, Bourgeois F, Karmouch J, MolgÃ³ J, Dobbertin A, Chevalier C, et al. Neuromuscular junction immaturity and muscle atrophy are hallmarks of the ColQ-deficient mouse, a model of congenital myasthenic syndrome with acetylcholinesterase deficiency. FASEB J. 2016;30:2382-99 pubmed publisher..Chevalier, C., Houlgatte, R., Léger, J., Legay, C. Neuromuscular junction immaturity and muscle atrophy are hallmarks of the ColQ-deficient mouse, a model of congenital myasthenic syndrome with acetylcholinesterase deficiency. ..
- Pandya K, Kim H, Smithies O. Fibrosis, not cell size, delineates beta-myosin heavy chain reexpression during cardiac hypertrophy and normal aging in vivo. Proc Natl Acad Sci U S A. 2006;103:16864-9 pubmed..We conclude that beta-MHC gene expression in the normal aging adult and hypertrophic mouse heart is a marker of fibrosis rather than of cellular hypertrophy. ..
- Ishibashi Y, Takahashi M, Isomatsu Y, Qiao F, Iijima Y, Shiraishi H, et al. Role of microtubules versus myosin heavy chain isoforms in contractile dysfunction of hypertrophied murine cardiocytes. Am J Physiol Heart Circ Physiol. 2003;285:H1270-85 pubmed
- Koga H, Kaji Y, Nishii K, Shirai M, Tomotsune D, Osugi T, et al. Overexpression of Polycomb-group gene rae28 in cardiomyocytes does not complement abnormal cardiac morphogenesis in mice lacking rae28 but causes dilated cardiomyopathy. Lab Invest. 2002;82:375-85 pubmed..rae28-induced dilated cardiomyopathy may thus provide a clue for clarifying the direct role of PcG in the maintenance of cardiomyocytes. ..
- Yamak A, Temsah R, Maharsy W, Caron S, Paradis P, Aries A, et al. Cyclin D2 rescues size and function of GATA4 haplo-insufficient hearts. Am J Physiol Heart Circ Physiol. 2012;303:H1057-66 pubmed publisher..The finding that postnatal upregulation of a cell-cycle gene in GATA4 haplo-insufficient hearts may be protective opens new avenues for maintaining or restoring cardiac function in GATA4-dependent cardiac disease. ..
- Stark D, Coffey N, Pancoast H, Arnold L, Walker J, VallÃ©e J, et al. Ephrin-A3 promotes and maintains slow muscle fiber identity during postnatal development and reinnervation. J Cell Biol. 2015;211:1077-91 pubmed publisher..We therefore conclude that Eph/ephrin interactions guide the fiber type specificity of neuromuscular interactions during development and adult life. ..
- Park I, Han C, Jin S, Lee B, Choi H, Kwon J, et al. Myosin regulatory light chains are required to maintain the stability of myosin II and cellular integrity. Biochem J. 2011;434:171-80 pubmed publisher..Taken together, our study provides direct evidence that normal levels of non-muscle RLCs are essential for maintaining the integrity of myosin II, and indicates that the RLCs are critical for cell structure and dynamics. ..
- Luxan G, Casanova J, Martínez Poveda B, Prados B, D Amato G, MacGrogan D, et al. Mutations in the NOTCH pathway regulator MIB1 cause left ventricular noncompaction cardiomyopathy. Nat Med. 2013;19:193-201 pubmed publisher..These results implicate NOTCH signaling in LVNC and indicate that MIB1 mutations arrest chamber myocardium development, preventing trabecular maturation and compaction. ..
- Hu J, McGlinn E, Harfe B, Kardon G, Tabin C. Autonomous and nonautonomous roles of Hedgehog signaling in regulating limb muscle formation. Genes Dev. 2012;26:2088-102 pubmed publisher..We identify neuroepithelial cell transforming gene 1 (Net1) as a downstream target and effector of Shh signaling in that context. ..
- Kasahara A, Cipolat S, Chen Y, Dorn G, Scorrano L. Mitochondrial fusion directs cardiomyocyte differentiation via calcineurin and Notch signaling. Science. 2013;342:734-7 pubmed publisher..Orchestration of cardiomyocyte differentiation by mitochondrial morphology reveals how mitochondria, Ca(2+), and calcineurin interact to regulate Notch1 signaling. ..
- Stopp S, Gründl M, Fackler M, Malkmus J, Leone M, Naumann R, et al. Deletion of Gas2l3 in mice leads to specific defects in cardiomyocyte cytokinesis during development. Proc Natl Acad Sci U S A. 2017;114:8029-8034 pubmed publisher..Together these results suggest that GAS2L3 plays a specific role in cardiomyocyte cytokinesis and proliferation during heart development. ..
- Knotts S, Rindt H, Neumann J, Robbins J. In vivo regulation of the mouse beta myosin heavy chain gene. J Biol Chem. 1994;269:31275-82 pubmed..However, simultaneous mutation of the three sites significantly reduces expression, indicating that these conserved sequences do play an important role and that combinatorial interactions underlie the beta MyHC's regulation. ..
- GÃ³rnikiewicz B, Ronowicz A, KrzemiÅ„ski M, Sachadyn P. Changes in gene methylation patterns in neonatal murine hearts: Implications for the regenerative potential. BMC Genomics. 2016;17:231 pubmed publisher..This conclusion is supported by the evidence that an increase in DNA methylation in the neonatal murine heart from day 1 to day 7 occurs in the promoter regions of genes playing important roles in cardiovascular system development. ..
- Bertrand A, Renou L, Papadopoulos A, Beuvin M, Lacene E, Massart C, et al. DelK32-lamin A/C has abnormal location and induces incomplete tissue maturation and severe metabolic defects leading to premature death. Hum Mol Genet. 2012;21:1037-48 pubmed publisher..And importantly, L-CMD patients should be investigated for putative metabolic disorders. ..
- Gloss B, Sayen M, Trost S, Bluhm W, Meyer M, Swanson E, et al. Altered cardiac phenotype in transgenic mice carrying the delta337 threonine thyroid hormone receptor beta mutant derived from the S family. Endocrinology. 1999;140:897-902 pubmed..Changes in cardiac gene expression, cardiac muscle contractility, and electrocardiogram are compatible with a hypothyroid cardiac phenotype despite normal T3 levels, indicating a dominant negative effect of the T3Rbeta mutant. ..
- Moorman A, Houweling A, de Boer P, Christoffels V. Sensitive nonradioactive detection of mRNA in tissue sections: novel application of the whole-mount in situ hybridization protocol. J Histochem Cytochem. 2001;49:1-8 pubmed..The radioactive ISH procedure scarcely permitted detection of these sequences, underscoring the value of this novel method. ..
- Angrisano T, Schiattarella G, Keller S, Pironti G, Florio E, Magliulo F, et al. Epigenetic switch at atp2a2 and myh7 gene promoters in pressure overload-induced heart failure. PLoS ONE. 2014;9:e106024 pubmed publisher..of the sarcoplasmic reticulum Ca2+ATPase (SERCA-2A) and Î²-myosin-heavy chain (Î²-MHC) genes (Atp2a2 and Myh7, respectively) in murine hearts after one or eight weeks of pressure overload induced by transverse aortic ..
- Hattori K, Nakamura K, Hisatomi Y, Matsumoto S, Suzuki M, Harvey R, et al. Arrhythmia induced by spatiotemporal overexpression of calreticulin in the heart. Mol Genet Metab. 2007;91:285-93 pubmed..Our findings support calreticulin being critical for normal heart function and structure. These mice are a useful model for the study of endoplasmic reticulum proteins, such as calreticulin, in various tissues. ..
- Zakariyah A, Rajgara R, Veinot J, Skerjanc I, Burgon P. Congenital heart defect causing mutation in Nkx2.5 displays in vivo functional deficit. J Mol Cell Cardiol. 2017;105:89-98 pubmed publisher..Collectively, the present study demonstrates that mice with the R141C point mutation in the Nkx2.5 allele phenocopies humans with the NKX2.5 R142C point mutation. ..
- Vieira J, Howard S, Villa del Campo C, Bollini S, Dubé K, Masters M, et al. BRG1-SWI/SNF-dependent regulation of the Wt1 transcriptional landscape mediates epicardial activity during heart development and disease. Nat Commun. 2017;8:16034 pubmed publisher..These findings reveal essential functions for chromatin-remodelling in the activation of EPDCs during cardiovascular development and repair. ..
- Nguyen A, Xiao B, Neppl R, Kallin E, Li J, Chen T, et al. DOT1L regulates dystrophin expression and is critical for cardiac function. Genes Dev. 2011;25:263-74 pubmed publisher..In addition, our study may open new avenues for the diagnosis and treatment of human heart disease. ..
- Yuan B, Wan P, Chu D, Nie J, Cao Y, Luo W, et al. A cardiomyocyte-specific Wdr1 knockout demonstrates essential functional roles for actin disassembly during myocardial growth and maintenance in mice. Am J Pathol. 2014;184:1967-80 pubmed publisher..Taken together, these results demonstrate that AIP1-regulated actin dynamics play essential roles in heart function in mice. ..
- Yin Z, Jones G, Towns W, Zhang X, Abel E, Binkley P, et al. Heart-specific ablation of Prkar1a causes failure of heart development and myxomagenesis. Circulation. 2008;117:1414-22 pubmed publisher..These biochemical changes lead to myxoma-like changes, indicating that these mice may be a good model with which to study the formation of these tumors. ..
- Lyons G, Ontell M, Cox R, Sassoon D, Buckingham M. The expression of myosin genes in developing skeletal muscle in the mouse embryo. J Cell Biol. 1990;111:1465-76 pubmed..The data presented are the first detailed study of myosin gene expression at these early stages of skeletal muscle development. ..
- Colbert M, Kirby M, Robbins J. Endogenous retinoic acid signaling colocalizes with advanced expression of the adult smooth muscle myosin heavy chain isoform during development of the ductus arteriosus. Circ Res. 1996;78:790-8 pubmed..These data suggest that RA may play a role in inducing and maintaining smooth muscle differentiation in the developing ductus arteriosus and may promote precocious expression of the adult vascular phenotype. ..
- Franco D, Markman M, Wagenaar G, Ya J, Lamers W, Moorman A. Myosin light chain 2a and 2v identifies the embryonic outflow tract myocardium in the developing rodent heart. Anat Rec. 1999;254:135-46 pubmed..These findings demonstrate the contribution of the outflow tract to the definitive ventricles and demonstrate that the outlet septum is derived from outflow tract myocardium. ..
- Thompson W, Nadal Ginard B, Mahdavi V. A MyoD1-independent muscle-specific enhancer controls the expression of the beta-myosin heavy chain gene in skeletal and cardiac muscle cells. J Biol Chem. 1991;266:22678-88 pubmed..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. ..
- Ruiz J, Conlon F, Robertson E. Identification of novel protein kinases expressed in the myocardium of the developing mouse heart. Mech Dev. 1994;48:153-64 pubmed..75-8.5 dpc developing heart. Subsequently, msk mRNA expression is rapidly downregulated. The patterns of Hek2 and msk expression suggest that these protein kinases may function during development of the primitive heart. ..
- Jones W, Sanchez A, Robbins J. Murine pulmonary myocardium: developmental analysis of cardiac gene expression. Dev Dyn. 1994;200:117-28 pubmed
- Zhao W, Zhao T, Chen Y, Zhao F, Gu Q, Williams R, et al. A Murine Hypertrophic Cardiomyopathy Model: The DBA/2J Strain. PLoS ONE. 2015;10:e0133132 pubmed publisher..HCM) is attributed to mutations in genes that encode for the sarcomere proteins, especially Mybpc3 and Myh7. Genotype-phenotype correlation studies show significant variability in HCM phenotypes among affected individuals ..
- Schoenauer R, Lange S, Hirschy A, Ehler E, Perriard J, Agarkova I. Myomesin 3, a novel structural component of the M-band in striated muscle. J Mol Biol. 2008;376:338-51 pubmed publisher..We propose that each member of the myomesin family is a component of one of the distinct ultrastructures, the M-lines, which modulate the mechanical properties of the M-bands in different muscle types. ..
- Waller B, McQuinn T, Phelps A, Markwald R, Lo C, Thompson R, et al. Conotruncal anomalies in the trisomy 16 mouse: an immunohistochemical analysis with emphasis on the involvement of the neural crest. Anat Rec. 2000;260:279-93 pubmed..Our observations strongly suggest that abnormal neural crest cell behavior is involved in the pathogenesis of the conotruncal malformations in the Ts16 mouse. ..
- Arai A, Yamamoto K, Toyama J. Murine cardiac progenitor cells require visceral embryonic endoderm and primitive streak for terminal differentiation. Dev Dyn. 1997;210:344-53 pubmed..5 days p.c., as a consequence of the multistep induction by cell interactions with both the primitive streak and visceral embryonic endoderm, following the genetic specification to cardiac lineage in the early gastrula stage. ..
- NÃ¼hrenberg T, Hammann N, Schnick T, PreiÃŸl S, Witten A, Stoll M, et al. Cardiac Myocyte De Novo DNA Methyltransferases 3a/3b Are Dispensable for Cardiac Function and Remodeling after Chronic Pressure Overload in Mice. PLoS ONE. 2015;10:e0131019 pubmed publisher..The absence of cardiac pathology in the presence of the predicted molecular phenotype suggests that de novo DNA methylation in cardiomyocytes is dispensable for adaptive mechanisms after chronic cardiac pressure overload. ..
- Kamaludin A, Smolarchuk C, Bischof J, Eggert R, Greer J, Ren J, et al. Muscle dysfunction caused by loss of Magel2 in a mouse model of Prader-Willi and Schaaf-Yang syndromes. Hum Mol Genet. 2016;25:3798-3809 pubmed publisher..Magel2-null mice serve as a preclinical model for therapies targeting muscle structure and function in children lacking MAGEL2 diagnosed with Prader-Willi or Schaaf-Yang syndrome. ..
- Lyons G, Schiaffino S, Sassoon D, Barton P, Buckingham M. Developmental regulation of myosin gene expression in mouse cardiac muscle. J Cell Biol. 1990;111:2427-36 pubmed..This dynamic pattern of changes in the myosin phenotype in the prenatal mouse heart suggests that there are different regulatory mechanisms for cell-specific expression of myosin isoforms during cardiac development. ..
- Qiu Z, Cang Y, Goff S. c-Abl tyrosine kinase regulates cardiac growth and development. Proc Natl Acad Sci U S A. 2010;107:1136-41 pubmed publisher..Genes involved in cardiac stress and remodeling and cell cycle regulation are also up-regulated in the mutant hearts. These findings reveal an essential role for c-Abl in mammalian heart growth and development. ..