Myosin Heavy Chains
"Myosin Heavy Chains" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
The larger subunits of MYOSINS. The heavy chains have a molecular weight of about 230 kDa and each heavy chain is usually associated with a dissimilar pair of MYOSIN LIGHT CHAINS. The heavy chains possess actin-binding and ATPase activity.
Descriptor ID |
D018995
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MeSH Number(s) |
D05.750.078.730.475.100 D08.811.277.040.025.193.750.249 D12.776.210.500.600.100 D12.776.220.525.475.100
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Concept/Terms |
Myosin Heavy Chains- Myosin Heavy Chains
- Heavy Chains, Myosin
- Myosin Heavy Chain
- Heavy Chain, Myosin
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Below are MeSH descriptors whose meaning is more general than "Myosin Heavy Chains".
Below are MeSH descriptors whose meaning is more specific than "Myosin Heavy Chains".
This graph shows the total number of publications written about "Myosin Heavy Chains" by people in this website by year, and whether "Myosin Heavy Chains" was a major or minor topic of these publications.
To see the data from this visualization as text, click here.
Year | Major Topic | Minor Topic | Total |
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2002 | 1 | 0 | 1 | 2004 | 0 | 1 | 1 | 2005 | 0 | 1 | 1 | 2006 | 0 | 1 | 1 | 2008 | 1 | 0 | 1 | 2009 | 1 | 1 | 2 | 2010 | 0 | 1 | 1 | 2015 | 0 | 1 | 1 |
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Below are the most recent publications written about "Myosin Heavy Chains" by people in Profiles.
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Babcock LW, Knoblauch M, Clarke MS. The role of myostatin and activin receptor IIB in the regulation of unloading-induced myofiber type-specific skeletal muscle atrophy. J Appl Physiol (1985). 2015 Sep 15; 119(6):633-42.
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Gajewski KM, Schulz RA. CF2 represses Actin 88F gene expression and maintains filament balance during indirect flight muscle development in Drosophila. PLoS One. 2010 May 25; 5(5):e10713.
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Abu-Daya A, Sater AK, Wells DE, Mohun TJ, Zimmerman LB. Absence of heartbeat in the Xenopus tropicalis mutation muzak is caused by a nonsense mutation in cardiac myosin myh6. Dev Biol. 2009 Dec 01; 336(1):20-9.
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Lombardi R, Dong J, Rodriguez G, Bell A, Leung TK, Schwartz RJ, Willerson JT, Brugada R, Marian AJ. Genetic fate mapping identifies second heart field progenitor cells as a source of adipocytes in arrhythmogenic right ventricular cardiomyopathy. Circ Res. 2009 May 08; 104(9):1076-84.
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Millman EE, Zhang H, Zhang H, Godines V, Bean AJ, Knoll BJ, Moore RH. Rapid recycling of beta-adrenergic receptors is dependent on the actin cytoskeleton and myosin Vb. Traffic. 2008 Nov; 9(11):1958-71.
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Oka T, Maillet M, Watt AJ, Schwartz RJ, Aronow BJ, Duncan SA, Molkentin JD. Cardiac-specific deletion of Gata4 reveals its requirement for hypertrophy, compensation, and myocyte viability. Circ Res. 2006 Mar 31; 98(6):837-45.
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Gajewski KM, Wang J, Schulz RA. Calcineurin function is required for myofilament formation and troponin I isoform transition in Drosophila indirect flight muscle. Dev Biol. 2006 Jan 01; 289(1):17-29.
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Wei L, Taffet GE, Khoury DS, Bo J, Li Y, Yatani A, Delaughter MC, Klevitsky R, Hewett TE, Robbins J, Michael LH, Schneider MD, Entman ML, Schwartz RJ. Disruption of Rho signaling results in progressive atrioventricular conduction defects while ventricular function remains preserved. FASEB J. 2004 May; 18(7):857-9.
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Semsarian C, Ahmad I, Giewat M, Georgakopoulos D, Schmitt JP, McConnell BK, Reiken S, Mende U, Marks AR, Kass DA, Seidman CE, Seidman JG. The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model. J Clin Invest. 2002 Apr; 109(8):1013-20.
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