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MeSH Review


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Disease relevance of Sarcomeres


Psychiatry related information on Sarcomeres


High impact information on Sarcomeres

  • Unexpectedly, in addition to loss of Tnnt2 expression in sih mutant hearts, we observed a significant reduction in Tpma and Tnni3, and consequently, severe sarcomere defects [6].
  • Cardiac troponin T is essential in sarcomere assembly and cardiac contractility [6].
  • Because distinct mutations in sarcomere proteins cause either dilated or hypertrophic cardiomyopathy, the effects of mutant sarcomere proteins on muscle mechanics must trigger two different series of events that remodel the heart [7].
  • Because alpha-tropomyosin and cardiac troponin T as well as beta myosin heavy chain mutations cause the same phenotype, we conclude that FHC is a disease of the sarcomere [8].
  • Twelve mutants in the unc-52 II gene exhibit markedly retarded sarcomere construction and progressive paralysis [9].

Chemical compound and disease context of Sarcomeres

  • Cardiac hypertrophy due to a chronic hemodynamic overload is accompanied by isoformic changes of two proteins of the thick filament of the sarcomere, myosin, and creatine phosphokinase [10].
  • Maximum contraction amplitudes (sarcomere length change, micron) with isoproterenol before pertussis toxin were 0.144 +/- 0.011 (Y, n = 22 animals), 0.104 +/- 0.009 (A. 18) and 0.098 +/- 0.009 (S. 14), P < 0.01 by analysis of variance (ANOVA) [11].
  • To determine whether changes in sarcomere length affect the inotropic response of the heart to angiotensin II (ANG II) differently in dilated and failing myocardium, papillary muscles were removed 2 days after infarction, and the effects of ANG II were studied at various muscle lengths [12].
  • Furthermore, activation of protein kinase Cepsilon (PKCepsilon) was necessary for length recovery, as nonselective PKC inhibitors [staurosporine (5 micromol/L) and chelerythrine chloride (10 micromol/L)], and a replication-defective adenovirus (Adv) encoding a dominant-negative mutant of PKCepsilon prevented the restoration of sarcomere length [13].

Biological context of Sarcomeres


Anatomical context of Sarcomeres

  • The individual units of the sarcomere, the basic contractile unit of myofibrils, include the thin, thick, titin, and nebulin filaments [19].
  • We used single sarcomeres from which the Z-lines, structures which anchor the thin filaments in the sarcomere, had been completely removed by calcium-activated neutral protease (CANP) and trypsin, and measured both the sliding velocity of single actin filaments along myosin filaments and the ATPase activity during sliding [20].
  • We hypothesize that ACTC mutations affecting sarcomere contraction lead to FHC and that mutations affecting force transmission from the sarcomere to the surrounding syncytium lead to IDC [21].
  • Nebulin, a giant myofibrillar protein (600-800 kD) that is abundant (3%) in the sarcomere of a wide range of skeletal muscles, has been proposed as a component of a cytoskeletal matrix that coexists with actin and myosin filaments within the sarcomere [22].
  • Using dominant-negative approaches in cardiac myocytes, both the titin Z1-Z2 domains and titin-cap are shown to be required for the structural integrity of sarcomeres, suggesting that their interaction is critical in titin filament-regulated sarcomeric assembly [23].

Associations of Sarcomeres with chemical compounds

  • Titin and/or nebulin apparently provide axial continuity for the production of resting tension on stretch and also tend to keep the thick filaments centred within the sarcomere during force generation [24].
  • Several hypertrophic agonists, such as angiotensin II, phenylephrine, and endothelin-1, have been shown to promote the sarcomere organization [25].
  • Analysis of small areas of I-band and large areas, including several sarcomeres, suggested that chloride is anisotropically distributed, with some of it probably bound to myosin [26].
  • The location of the threefold symmetric connection C4, relative to the thick filament of the adjacent sarcomere, is determined and its possible relationship to the C filament is considered [27].
  • The localization of high-molecular-weight (80,000-200,000-daltons) proteins in the sarcomere of striated muscle has been studied by coordinated electron-microscopic and sodium dodecyl sulfate (SDS) gel electrophoretic analysis of native myofilaments and extracted and digested myofibrils [28].

Gene context of Sarcomeres

  • First, we eliminated all actin or myosin in flight muscles to evaluate contributions of thick and thin filaments to sarcomere formation [29].
  • ET-1 also induced a significant increase in atrial natriuretic factor mRNA expression as well as in the percentage of cells with highly organized sarcomeres, responses which were also blocked by expression of SEK-1(KR) [30].
  • Absence of desmin filaments within the sarcomere does not interfere with primary muscle formation or regeneration [31].
  • In intact muscles flightin is associated with the A band of the sarcomere, where evidence suggests it interacts with the myosin filaments [32].
  • In the wild type, a constant ratio of the synthesis of the unc-54-coded myosin B to myosin A, about 2:1, is maintained during the larval stages in which the synthesis of both myosins increases exponentially and rapid sarcomere growth and addition ensues [33].

Analytical, diagnostic and therapeutic context of Sarcomeres


  1. Activated MEK5 induces serial assembly of sarcomeres and eccentric cardiac hypertrophy. Nicol, R.L., Frey, N., Pearson, G., Cobb, M., Richardson, J., Olson, E.N. EMBO J. (2001) [Pubmed]
  2. Reduced unloaded sarcomere shortening velocity and a shift to a slower myosin isoform in acute murine coxsackievirus myocarditis. Hamrell, B.B., Huber, S.A., Leslie, K.O. Circ. Res. (1994) [Pubmed]
  3. Amplification of the gli gene in childhood sarcomas. Roberts, W.M., Douglass, E.C., Peiper, S.C., Houghton, P.J., Look, A.T. Cancer Res. (1989) [Pubmed]
  4. Inherited disorders of contractile proteins in skeletal and cardiac muscle. Laing, N.G. Curr. Opin. Neurol. (1995) [Pubmed]
  5. Congenital myopathy with mosaic fibers and interlacing sarcomeres: a new structural myopathy. Marbini, A., Gemignani, F., Badiali, L., Bellanova, M.F., Margarito, F. Acta Neuropathol. (1998) [Pubmed]
  6. Cardiac troponin T is essential in sarcomere assembly and cardiac contractility. Sehnert, A.J., Huq, A., Weinstein, B.M., Walker, C., Fishman, M., Stainier, D.Y. Nat. Genet. (2002) [Pubmed]
  7. Mutations in sarcomere protein genes as a cause of dilated cardiomyopathy. Kamisago, M., Sharma, S.D., DePalma, S.R., Solomon, S., Sharma, P., McDonough, B., Smoot, L., Mullen, M.P., Woolf, P.K., Wigle, E.D., Seidman, J.G., Seidman, C.E. N. Engl. J. Med. (2000) [Pubmed]
  8. Alpha-tropomyosin and cardiac troponin T mutations cause familial hypertrophic cardiomyopathy: a disease of the sarcomere. Thierfelder, L., Watkins, H., MacRae, C., Lamas, R., McKenna, W., Vosberg, H.P., Seidman, J.G., Seidman, C.E. Cell (1994) [Pubmed]
  9. Muscle development in Caenorhabditis elegans: mutants exhibiting retarded sarcomere construction. Mackenzie, J.M., Garcea, R.L., Zengel, J.M., Epstein, H.F. Cell (1978) [Pubmed]
  10. Alpha-skeletal muscle actin mRNA's accumulate in hypertrophied adult rat hearts. Schwartz, K., de la Bastie, D., Bouveret, P., Oliviéro, P., Alonso, S., Buckingham, M. Circ. Res. (1986) [Pubmed]
  11. The role of Gi-proteins and beta-adrenoceptors in the age-related decline of contraction in guinea-pig ventricular myocytes. Ferrara, N., Böhm, M., Zolk, O., O'Gara, P., Harding, S.E. J. Mol. Cell. Cardiol. (1997) [Pubmed]
  12. Length-dependent modulation of ANG II inotropism in rat myocardium: effects of myocardial infarction. Li, P., Sonnenblick, E.H., Anversa, P., Capasso, J.M. Am. J. Physiol. (1994) [Pubmed]
  13. Restoration of resting sarcomere length after uniaxial static strain is regulated by protein kinase Cepsilon and focal adhesion kinase. Mansour, H., de Tombe, P.P., Samarel, A.M., Russell, B. Circ. Res. (2004) [Pubmed]
  14. Studies on cardiac myofibrillogenesis with antibodies to titin, actin, tropomyosin, and myosin. Wang, S.M., Greaser, M.L., Schultz, E., Bulinski, J.C., Lin, J.J., Lessard, J.L. J. Cell Biol. (1988) [Pubmed]
  15. The Caenorhabditis elegans vab-10 spectraplakin isoforms protect the epidermis against internal and external forces. Bosher, J.M., Hahn, B.S., Legouis, R., Sookhareea, S., Weimer, R.M., Gansmuller, A., Chisholm, A.D., Rose, A.M., Bessereau, J.L., Labouesse, M. J. Cell Biol. (2003) [Pubmed]
  16. Obscurin, a giant sarcomeric Rho guanine nucleotide exchange factor protein involved in sarcomere assembly. Young, P., Ehler, E., Gautel, M. J. Cell Biol. (2001) [Pubmed]
  17. Interference fine structure and sarcomere length dependence of the axial x-ray pattern from active single muscle fibers. Linari, M., Piazzesi, G., Dobbie, I., Koubassova, N., Reconditi, M., Narayanan, T., Diat, O., Irving, M., Lombardi, V. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  18. Paramyosin phosphorylation site disruption affects indirect flight muscle stiffness and power generation in Drosophila melanogaster. Liu, H., Miller, M.S., Swank, D.M., Kronert, W.A., Maughan, D.W., Bernstein, S.I. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  19. Striated muscle cytoarchitecture: an intricate web of form and function. Clark, K.A., McElhinny, A.S., Beckerle, M.C., Gregorio, C.C. Annu. Rev. Cell Dev. Biol. (2002) [Pubmed]
  20. Sliding distance of actin filament induced by a myosin crossbridge during one ATP hydrolysis cycle. Yanagida, T., Arata, T., Oosawa, F. Nature (1985) [Pubmed]
  21. Alpha-cardiac actin is a novel disease gene in familial hypertrophic cardiomyopathy. Mogensen, J., Klausen, I.C., Pedersen, A.K., Egeblad, H., Bross, P., Kruse, T.A., Gregersen, N., Hansen, P.S., Baandrup, U., Borglum, A.D. J. Clin. Invest. (1999) [Pubmed]
  22. Architecture of the sarcomere matrix of skeletal muscle: immunoelectron microscopic evidence that suggests a set of parallel inextensible nebulin filaments anchored at the Z line. Wang, K., Wright, J. J. Cell Biol. (1988) [Pubmed]
  23. The NH2 terminus of titin spans the Z-disc: its interaction with a novel 19-kD ligand (T-cap) is required for sarcomeric integrity. Gregorio, C.C., Trombitás, K., Centner, T., Kolmerer, B., Stier, G., Kunke, K., Suzuki, K., Obermayr, F., Herrmann, B., Granzier, H., Sorimachi, H., Labeit, S. J. Cell Biol. (1998) [Pubmed]
  24. A physiological role for titin and nebulin in skeletal muscle. Horowits, R., Kempner, E.S., Bisher, M.E., Podolsky, R.J. Nature (1986) [Pubmed]
  25. Myosin light chain kinase mediates sarcomere organization during cardiac hypertrophy in vitro. Aoki, H., Sadoshima, J., Izumo, S. Nat. Med. (2000) [Pubmed]
  26. Calcium release and ionic changes in the sarcoplasmic reticulum of tetanized muscle: an electron-probe study. Somlyo, A.V., Gonzalez-Serratos, H.G., Shuman, H., McClellan, G., Somlyo, A.P. J. Cell Biol. (1981) [Pubmed]
  27. Arrangement of filaments and cross-links in the bee flight muscle Z disk by image analysis of oblique sections. Deatherage, J.F., Cheng, N.Q., Bullard, B. J. Cell Biol. (1989) [Pubmed]
  28. Compositional studies of myofibrils from rabbit striated muscle. Etlinger, J.D., Zak, R., Fischman, D.A. J. Cell Biol. (1976) [Pubmed]
  29. Genetic dissection of Drosophila myofibril formation: effects of actin and myosin heavy chain null alleles. Beall, C.J., Sepanski, M.A., Fyrberg, E.A. Genes Dev. (1989) [Pubmed]
  30. Role of the stress-activated protein kinases in endothelin-induced cardiomyocyte hypertrophy. Choukroun, G., Hajjar, R., Kyriakis, J.M., Bonventre, J.V., Rosenzweig, A., Force, T. J. Clin. Invest. (1998) [Pubmed]
  31. Desmin is essential for the tensile strength and integrity of myofibrils but not for myogenic commitment, differentiation, and fusion of skeletal muscle. Li, Z., Mericskay, M., Agbulut, O., Butler-Browne, G., Carlsson, L., Thornell, L.E., Babinet, C., Paulin, D. J. Cell Biol. (1997) [Pubmed]
  32. Flightin, a novel myofibrillar protein of Drosophila stretch-activated muscles. Vigoreaux, J.O., Saide, J.D., Valgeirsdottir, K., Pardue, M.L. J. Cell Biol. (1993) [Pubmed]
  33. Mutants altering coordinate synthesis of specific myosins during nematode muscle development. Zengel, J.M., Epstein, H.F. Proc. Natl. Acad. Sci. U.S.A. (1980) [Pubmed]
  34. Cardiomyocytes can be generated from marrow stromal cells in vitro. Makino, S., Fukuda, K., Miyoshi, S., Konishi, F., Kodama, H., Pan, J., Sano, M., Takahashi, T., Hori, S., Abe, H., Hata, J., Umezawa, A., Ogawa, S. J. Clin. Invest. (1999) [Pubmed]
  35. Myopalladin, a novel 145-kilodalton sarcomeric protein with multiple roles in Z-disc and I-band protein assemblies. Bang, M.L., Mudry, R.E., McElhinny, A.S., Trombitás, K., Geach, A.J., Yamasaki, R., Sorimachi, H., Granzier, H., Gregorio, C.C., Labeit, S. J. Cell Biol. (2001) [Pubmed]
  36. Load regulation of the properties of adult feline cardiocytes. The role of substrate adhesion. Cooper, G., Mercer, W.E., Hoober, J.K., Gordon, P.R., Kent, R.L., Lauva, I.K., Marino, T.A. Circ. Res. (1986) [Pubmed]
  37. The effect of verapamil on the calcium paradox. Ruigrok, T.J., Boink, A.B., Slade, A., Zimmerman, A.N., Meijler, F.L., Nayler, W.G. Am. J. Pathol. (1980) [Pubmed]
  38. The hydrophilic domain of small ankyrin-1 interacts with the two N-terminal immunoglobulin domains of titin. Kontrogianni-Konstantopoulos, A., Bloch, R.J. J. Biol. Chem. (2003) [Pubmed]
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