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Myotubes

Figure 1. Muscle development. A skeletal muscle fiber is formed by the fusion of many single cells (myoblasts) into a multinucleated myotube. Myotubes then develop into the muscle fiber (see text). Sarcomeres form in longitudinal structures called myofibrils. The repeating structure of the sarcomere contains interdigitating thick and thin filaments. Figure 1. Muscle development. A skeletal muscle fiber is formed by the fusion of many single cells (myoblasts) into a multinucleated myotube. Myotubes then develop into the muscle fiber (see text). Sarcomeres form in longitudinal structures called myofibrils. The repeating structure of the sarcomere contains interdigitating thick and thin filaments.
Histopathological features are dominated by the large number of centrally-placed muscle nuclei, sometimes affecting more than 90% of muscle fibers. The nuclei form long chains in the middle of the fiber and are surrounded by cytoplasm, which contains mitochondria and membranous vesicles, but no myofibrils. This morphological appearance has prompted comparison with myotubes, and in fact centronuclear myopathies are sometimes referred to as myotubular myopathies. This is a misnomer, however, since although the affected fibers retain some of the structural features of myotubes, and maturational arrest may play a role in their formation, the vast majority of such fibers are fully differentiated histochemically into either type 1 or type 2. [Pg.294]

Endo, T. and Nidal-Ginard, B. (1988) SV40 large T antigen induces reentry of terminally differentiated myotubes into the cell cycle. In Kedes, L.H. and Stockdale, F.E. (eds) Cellular and Molecular Biology of Muscle Development. Alan R. Liss, New York, pp. 95-104. [Pg.142]

Cardiotrophin 1 acts as a survival factor for spinal motor neurons. CT-1 is synthesized by both skeletal muscle and myotubes and has been shown to be secreted from the latter, suggesting that it acts as a target-derived trophic factor. Indeed, in CT-1 knockout mice there is a loss of motor neurons in the spinal cord and brainstem [16]. CT-1 also promotes the survival of dopaminergic neurons and ciliary neurons. [Pg.478]

MASC myotube-associated specificity component NMR nuclear magnetic resonance... [Pg.965]

Velez, M., Barald, K. E., and Axelrod, D. (1990) Rotational diffusion of acetylcholine receptors on cultured rat myotubes. J. Cell Biol. 110, 2049-2059. [Pg.173]

Provided that blood supply and innervation remain intact, skeletal muscle heals well after injury or disease. Damage to fibres causes endothelial cells to secrete general growth factors (e.g. fibroblast growth factor, insulin-like growth factors) and growth factors specific to muscle development which stimulate proliferation of satellite cells. These then migrate to the site of injury to form myotubes, as in foetal development. If, however, the number of satellite cells is... [Pg.301]

Lee MS, Kim CH, Hoang DM, Kim BY, Sohn CB, Kim MR, Ahn JS. (2009) Genistein-derivatives from Tetracera scandens stimulate glucose-uptake in L6 myotubes. Biol Pharm Bull 32 504-508. [Pg.592]

Abdallah, . M., Beck-Nielsen, H., Gaster, M. (2005) Increased expression of 11(5-hydroxysteroid dehydrogenase type 1 in type 2 diabetic myotubes. Eur J Clin Invest 35, 627-634. [Pg.213]

Apart from AP-A, the best characterized of these polypeptides with respect to its biological activity is Anemonia sulcata toxin II (ATX II) [19]. This molecule is also cardioactive [28], as would be expected from its similarity to AP-A. Renaud et al. [29] have compared the activities of a number of sea anemone and scorpion toxins on isolated rat atria and found that anthopleurin-B (AP-B, also known as Ax II) had the highest potency and the greatest margin between the concentrations necessary for maximal inotropic activity and for provoking arrhythmias (0.3 versus 10 n . It was also found that sodium channels of rat cardiac cells in culture, which have a low affinity for tetrodotoxin (TTX), have a particularly high affinity for Type 1 anemone toxins [29], whereas Type 2 toxins [30] and scorpion toxins [31] had similar affinities for TTX-sensitive and TTX-insensitive channels in rat neuroblastoma cells and skeletal myotubes, respectively. [Pg.298]

Muscle, whose structure and function are discussed in Chapter 19, develops in response to four members of the myoD family. These include myoD, myogenin, myf5, and MRF4.417-419 All are muscle-specific transcription factors of the basic helix -loop -helix class. An unusual aspect of muscle development is formation of multinucleate myotubes (muscle fibers p. 1096)420 Apoptosis plays an important role in muscle development and can present significant complications in damaged cardiac muscle.421 Defects in several developmental control genes are responsible for congenital heart diseases.422... [Pg.1902]

Dowty, M.E., Williams, P., Zhang, G., Hangstrom, J.E. and Wolff, J.A. (1995) Plasmid DNA entry into post-mitotic nuclei of primary rat myotubes. Proc. Natl. Acad. Sci. USA, 92,4572-4576. [Pg.203]

Wolff, J.A., Dowty, M.E., Jiao, S., Repetto, R., Berg, R.K., Ludtke, J.J. et al. (1992a) Expression of naked plasmids by cultured myotubes and entry into T tubules and caveolae of mammalian skeletal muscle. J. Cell Sci., 103, 1249-1253. [Pg.234]

Sorci G, Bianchi R, Giambanco I, Rambotti MG, Donato R. 1999. Replicating myoblasts and fused myotubes express the calcium-regulated proteins S100A1 and S100B. Cell Calcium 25(2) 93-106. [Pg.135]

Morrill JA, Brown RH, Jr., Cannon SC (1998) Gating of the L-type Ca channel in human skeletal myotubes an activation defect caused by the hypokalemic periodic paralysis mutation R528H. J Neurosci 18 10320-10334. [Pg.249]

Sipos I, Jurkat-Rott K, Harasztosi C, Fontaine B, Kovacs L, Melzer W, Lehmann-Horn F(1995) Skeletal muscle DHP receptor mutations alter calcium currents in human hypokalaemic periodic paralysis myotubes. J Physiol 483 ( Pt 2) 299-306. [Pg.250]


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