sarcomeres

Summary

Summary: The repeating contractile units of the MYOFIBRIL, delimited by Z bands along its length.

Top Publications

  1. Wolny M, Colegrave M, Colman L, White E, Knight P, Peckham M. Cardiomyopathy mutations in the tail of ?-cardiac myosin modify the coiled-coil structure and affect integration into thick filaments in muscle sarcomeres in adult cardiomyocytes. J Biol Chem. 2013;288:31952-62 pubmed publisher
    ..and one dilated cardiomyopathy-causing (R1500W) tail mutations on their ability to incorporate into muscle sarcomeres in vivo...
  2. Rassier D, Pavlov I. Force produced by isolated sarcomeres and half-sarcomeres after an imposed stretch. Am J Physiol Cell Physiol. 2012;302:C240-8 pubmed publisher
    ..is disagreement if it represents a sarcomeric property, or if it is associated with length nonuniformities among sarcomeres and half-sarcomeres...
  3. Cornachione A, Rassier D. A non-cross-bridge, static tension is present in permeabilized skeletal muscle fibers after active force inhibition or actin extraction. Am J Physiol Cell Physiol. 2012;302:C566-74 pubmed publisher
    ..This finding indicates the existence of a Ca(2+)-regulated, titin-based stiffness in skeletal muscles...
  4. Tondon A, Hsu H, Kaunas R. Dependence of cyclic stretch-induced stress fiber reorientation on stretch waveform. J Biomech. 2012;45:728-35 pubmed publisher
    ..This integrated approach of experiment and theory provides new insight into the mechanisms by which cells respond to matrix stretching to maintain tensional homeostasis...
  5. Edman K. Residual force enhancement after stretch in striated muscle. A consequence of increased myofilament overlap?. J Physiol. 2012;590:1339-45 pubmed publisher
    ..that, dispersed in the preparation, there are assymetrical length changes within the two halves of myofibrillar sarcomeres resulting in greater filament overlap in one half of the sarcomere than in the opposite sarcomere half...
  6. Katzemich A, Kreisköther N, Alexandrovich A, Elliott C, Schock F, Leonard K, et al. The function of the M-line protein obscurin in controlling the symmetry of the sarcomere in the flight muscle of Drosophila. J Cell Sci. 2012;125:3367-79 pubmed publisher
    ..We conclude that obscurin in the IFM is necessary for the development of a symmetrical sarcomere in Drosophila IFM...
  7. 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...
  8. McNally E, Golbus J, Puckelwartz M. Genetic mutations and mechanisms in dilated cardiomyopathy. J Clin Invest. 2013;123:19-26 pubmed publisher
    ..Relatively few clinical clues guide the diagnosis of inherited DCM, but emerging evidence supports the use of genetic testing to identify those patients at risk for faster disease progression, congestive heart failure, and arrhythmia...
  9. Previs M, Beck Previs S, Gulick J, Robbins J, Warshaw D. Molecular mechanics of cardiac myosin-binding protein C in native thick filaments. Science. 2012;337:1215-8 pubmed publisher
    ..These results provide molecular insight into why cMyBP-C should be considered a member of a tripartite complex with actin and myosin that allows fine tuning of cardiac muscle contraction...

More Information

Publications76

  1. Lefta M, Campbell K, Feng H, Jin J, Esser K. Development of dilated cardiomyopathy in Bmal1-deficient mice. Am J Physiol Heart Circ Physiol. 2012;303:H475-85 pubmed publisher
  2. da Silva Lopes K, Pietas A, Radke M, Gotthardt M. Titin visualization in real time reveals an unexpected level of mobility within and between sarcomeres. J Cell Biol. 2011;193:785-98 pubmed publisher
    ..Our results suggest a model in which the largely unrestricted movement of titin within and between sarcomeres primarily depends on calcium, suggesting that fortification of the titin filament system is activity dependent.
  3. Minozzo F, Hilbert L, Rassier D. Pre-power-stroke cross-bridges contribute to force transients during imposed shortening in isolated muscle fibers. PLoS ONE. 2012;7:e29356 pubmed publisher
    ..Furthermore, the results of the model suggest that the mechanism by which blebbistatin inhibits force is by interfering with the closing of the myosin upper binding cleft, biasing cross-bridges into a pre-power-stroke state...
  4. Knoll R, Linke W, Zou P, Miocic S, Kostin S, Buyandelger B, et al. Telethonin deficiency is associated with maladaptation to biomechanical stress in the mammalian heart. Circ Res. 2011;109:758-69 pubmed publisher
    ..In addition, a variety of telethonin mutations are associated with the development of several different diseases; however, little is known about the underlying molecular mechanisms and telethonin's in vivo function...
  5. Razzaque M, Gupta M, Osinska H, Gulick J, Blaxall B, Robbins J. An endogenously produced fragment of cardiac myosin-binding protein C is pathogenic and can lead to heart failure. Circ Res. 2013;113:553-61 pubmed publisher
    ..Elevated levels of the fragment can be detected in the diseased mouse and human heart, but its ability to interfere with normal cardiac function in the intact animal is unexplored...
  6. Serizawa T, Terui T, Kagemoto T, Mizuno A, Shimozawa T, Kobirumaki F, et al. Real-time measurement of the length of a single sarcomere in rat ventricular myocytes: a novel analysis with quantum dots. Am J Physiol Cell Physiol. 2011;301:C1116-27 pubmed publisher
    As the dynamic properties of cardiac sarcomeres are markedly changed in response to a length change of even ?0.1 ?m, it is imperative to quantitatively measure sarcomere length (SL)...
  7. Cohen S, Zhai B, Gygi S, Goldberg A. Ubiquitylation by Trim32 causes coupled loss of desmin, Z-bands, and thin filaments in muscle atrophy. J Cell Biol. 2012;198:575-89 pubmed publisher
    ..Thus, during fasting, desmin phosphorylation increases and enhances Trim32-mediated degradation of the desmin cytoskeleton, which appears to facilitate the breakdown of Z-bands and thin filaments...
  8. Chung C, Methawasin M, Nelson O, Radke M, Hidalgo C, Gotthardt M, et al. Titin based viscosity in ventricular physiology: an integrative investigation of PEVK-actin interactions. J Mol Cell Cardiol. 2011;51:428-34 pubmed publisher
    ..This integrative study is the first to quantify the influence of a specific molecular (PEVK-actin) viscosity in vivo and shows that PEVK-actin interactions are an important physiological source of viscosity...
  9. Melkani G, Bodmer R, Ocorr K, Bernstein S. The UNC-45 chaperone is critical for establishing myosin-based myofibrillar organization and cardiac contractility in the Drosophila heart model. PLoS ONE. 2011;6:e22579 pubmed publisher
  10. Just S, Meder B, Berger I, Etard C, Trano N, Patzel E, et al. The myosin-interacting protein SMYD1 is essential for sarcomere organization. J Cell Sci. 2011;124:3127-36 pubmed publisher
    Assembly, maintenance and renewal of sarcomeres require highly organized and balanced folding, transport, modification and degradation of sarcomeric proteins. However, the molecules that mediate these processes are largely unknown...
  11. Craig E, Dey S, Mogilner A. The emergence of sarcomeric, graded-polarity and spindle-like patterns in bundles of short cytoskeletal polymers and two opposite molecular motors. J Phys Condens Matter. 2011;23:374102 pubmed publisher
    ..We discuss modeling implications for actin-myosin fibers and in vitro and meiotic spindles...
  12. Campbell S, Hatfield P, Campbell K. A mathematical model of muscle containing heterogeneous half-sarcomeres exhibits residual force enhancement. PLoS Comput Biol. 2011;7:e1002156 pubmed publisher
    ..We hypothesized that residual force enhancement could reflect mechanical interactions between heterogeneous half-sarcomeres. To test this hypothesis, we subjected a computational model of interacting heterogeneous half-sarcomeres to the ..
  13. Conover G, Gregorio C. The desmin coil 1B mutation K190A impairs nebulin Z-disc assembly and destabilizes actin thin filaments. J Cell Sci. 2011;124:3464-76 pubmed publisher
    ..Desmin attaches to sarcomeres through its high-affinity association with nebulin, a giant F-actin binding protein that co-extends along the ..
  14. Witjas Paalberends E, Piroddi N, Stam K, Van Dijk S, Oliviera V, Ferrara C, et al. Mutations in MYH7 reduce the force generating capacity of sarcomeres in human familial hypertrophic cardiomyopathy. Cardiovasc Res. 2013;99:432-41 pubmed publisher
    ..We studied whether cellular dysfunction is due to an intrinsic sarcomere defect or cardiomyocyte remodelling...
  15. Seidman C, Seidman J. Identifying sarcomere gene mutations in hypertrophic cardiomyopathy: a personal history. Circ Res. 2011;108:743-50 pubmed publisher
  16. Knoll R, Buyandelger B, Lab M. The sarcomeric Z-disc and Z-discopathies. J Biomed Biotechnol. 2011;2011:569628 pubmed publisher
    ..This paper provides a brief overview of these novel aspects as well as points to future research directions...
  17. Posch M, Waldmüller S, Muller M, Scheffold T, Fournier D, Andrade Navarro M, et al. Cardiac alpha-myosin (MYH6) is the predominant sarcomeric disease gene for familial atrial septal defects. PLoS ONE. 2011;6:e28872 pubmed publisher
    ..In particular, perturbations in the MYH6 head domain seem to play a major role in the genetic origin of familial ASDII...
  18. Friedrich B, Fischer Friedrich E, Gov N, Safran S. Sarcomeric pattern formation by actin cluster coalescence. PLoS Comput Biol. 2012;8:e1002544 pubmed publisher
    ..The proposed mechanism could be generic and apply both to premyofibrils and nascent myofibrils in developing muscle cells as well as possibly to striated stress-fibers in non-muscle cells...
  19. Marston S. How do mutations in contractile proteins cause the primary familial cardiomyopathies?. J Cardiovasc Transl Res. 2011;4:245-55 pubmed publisher
    ..A plausible link between uncoupling and DCM has been proposed via blunting of the response to ?-adrenergic stimulation...
  20. McDonald K. The interdependence of Ca2+ activation, sarcomere length, and power output in the heart. Pflugers Arch. 2011;462:61-7 pubmed publisher
  21. Irving T, Wu Y, Bekyarova T, Farman G, Fukuda N, Granzier H. Thick-filament strain and interfilament spacing in passive muscle: effect of titin-based passive tension. Biophys J. 2011;100:1499-508 pubmed publisher
    ..This difference can be explained by the fact that thick filaments are more compliant at low tension (passive muscle) than at high tension (tetanic tension). The implications of our findings are discussed...
  22. Frank D, Frey N. Cardiac Z-disc signaling network. J Biol Chem. 2011;286:9897-904 pubmed publisher
    ..This minireview thus focuses on novel components and recent developments in z-disc biology and their role in cardiac signaling and disease...
  23. Rassier D. The mechanisms of the residual force enhancement after stretch of skeletal muscle: non-uniformity in half-sarcomeres and stiffness of titin. Proc Biol Sci. 2012;279:2705-13 pubmed publisher
    ..This paper reviews studies performed with single muscle fibres, myofibrils and sarcomeres to investigate the mechanisms of the stretch-induced force enhancement...
  24. Portbury A, Willis M, Patterson C. Tearin' up my heart: proteolysis in the cardiac sarcomere. J Biol Chem. 2011;286:9929-34 pubmed publisher
    ..This minireview focuses on the individual as well as cooperative involvement of each of these three major pathways of proteolysis within the cardiac sarcomere...
  25. Maron B, Maron M, Semsarian C. Double or compound sarcomere mutations in hypertrophic cardiomyopathy: a potential link to sudden death in the absence of conventional risk factors. Heart Rhythm. 2012;9:57-63 pubmed publisher
    ..Therefore, additional genetic risk markers that reliably determine which patients are predisposed to sudden death are needed...
  26. Grosberg A, Kuo P, Guo C, Geisse N, Bray M, Adams W, et al. Self-organization of muscle cell structure and function. PLoS Comput Biol. 2011;7:e1001088 pubmed publisher
  27. Sumandea M, Steinberg S. Redox signaling and cardiac sarcomeres. J Biol Chem. 2011;286:9921-7 pubmed publisher
    ..This minireview focuses on myofilament protein post-translational modifications induced by ROS or ROS-activated signaling enzymes that regulate cardiac contractility...
  28. Govindan S, McElligott A, Muthusamy S, Nair N, Barefield D, Martin J, et al. Cardiac myosin binding protein-C is a potential diagnostic biomarker for myocardial infarction. J Mol Cell Cardiol. 2012;52:154-64 pubmed publisher
    ..The presence of elevated levels of cMyBP-C in the blood provides a promising novel biomarker able to accurately rule in MI, thus aiding in the further assessment of ischemic heart disease...
  29. Lund L, Kerr J, Lupinetti J, Zhang Y, Russell M, Bloch R, et al. Synemin isoforms differentially organize cell junctions and desmin filaments in neonatal cardiomyocytes. FASEB J. 2012;26:137-48 pubmed publisher
    ..We conclude that ?-synemin mediates the association of desmin IFs with Z disks, whereas ?-synemin stabilizes junctional complexes between cardiomyocytes...
  30. Lakdawala N, Thune J, Maron B, Cirino A, Havndrup O, Bundgaard H, et al. Electrocardiographic features of sarcomere mutation carriers with and without clinically overt hypertrophic cardiomyopathy. Am J Cardiol. 2011;108:1606-13 pubmed publisher
    ..However, owing to the limited sensitivity of ECG and echocardiographic screening, genetic testing is required to definitively identify at-risk family members...
  31. Kuo P, Lee H, Bray M, Geisse N, Huang Y, Adams W, et al. Myocyte shape regulates lateral registry of sarcomeres and contractility. Am J Pathol. 2012;181:2030-7 pubmed publisher
    ..Our data suggest that cell shape is critical in determining contractile performance of single cardiomyocytes by regulating the intracellular structure and calcium handling ability...
  32. Govindan S, Sarkey J, Ji X, Sundaresan N, Gupta M, de Tombe P, et al. Pathogenic properties of the N-terminal region of cardiac myosin binding protein-C in vitro. J Muscle Res Cell Motil. 2012;33:17-30 pubmed publisher
    ..By elucidating the deleterious effects of endogenously expressed cMyBP-C N-terminal fragments on sarcomere function, these data contribute to the understanding of contractile dysfunction following myocardial injury. ..
  33. Chapin L, Blankman E, Smith M, Shiu Y, Beckerle M. Lateral communication between stress fiber sarcomeres facilitates a local remodeling response. Biophys J. 2012;103:2082-92 pubmed publisher
    ..Using fluorescently tagged zyxin to track the borders of sarcomeres, we characterize the dynamics of resting sarcomeres and strain-site sarcomeres...
  34. Abdul Hussein S, van der Ven P, Tajsharghi H. Expression profiles of muscle disease-associated genes and their isoforms during differentiation of cultured human skeletal muscle cells. BMC Musculoskelet Disord. 2012;13:262 pubmed publisher
    ..It is likely that elucidation of the expression patterns of muscle-specific sarcomeric proteins is important to understand muscle disorders originating from defects in contractile sarcomeric proteins...
  35. Gokhin D, Fowler V. A two-segment model for thin filament architecture in skeletal muscle. Nat Rev Mol Cell Biol. 2013;14:113-9 pubmed publisher
    ..The two-segment model implicates position-specific microregulation of actin dynamics as a general principle underlying actin filament length and stability...
  36. Roncarati R, Latronico M, Musumeci B, Aurino S, Torella A, Bang M, et al. Unexpectedly low mutation rates in beta-myosin heavy chain and cardiac myosin binding protein genes in Italian patients with hypertrophic cardiomyopathy. J Cell Physiol. 2011;226:2894-900 pubmed publisher
    ..This finding, coupled to the clinical diversity of our cohort, emphasizes the complexity of HCM and the need for more inclusive investigative approaches in order to fully understand the pathogenesis of this disease...
  37. Kamm K, Stull J. Signaling to myosin regulatory light chain in sarcomeres. J Biol Chem. 2011;286:9941-7 pubmed publisher
  38. Massa R, Panico M, Caldarola S, Fusco F, Sabatelli P, Terracciano C, et al. The myotonic dystrophy type 2 (DM2) gene product zinc finger protein 9 (ZNF9) is associated with sarcomeres and normally localized in DM2 patients' muscles. Neuropathol Appl Neurobiol. 2010;36:275-84 pubmed publisher
    ..The aim of the present work was therefore to assess ZNF9 protein expression in rat tissues and in human muscle, and ZNF9 subcellular distribution in normal and DM2 human muscles...
  39. Kontrogianni Konstantopoulos A, Ackermann M, Bowman A, Yap S, Bloch R. Muscle giants: molecular scaffolds in sarcomerogenesis. Physiol Rev. 2009;89:1217-67 pubmed publisher
    ..and integration of a large number of contractile, cytoskeletal, and signaling proteins into regular arrays, the sarcomeres. It is also associated with the stereotypical assembly of the sarcoplasmic reticulum and the transverse tubules ..
  40. Ono S. Dynamic regulation of sarcomeric actin filaments in striated muscle. Cytoskeleton (Hoboken). 2010;67:677-92 pubmed publisher
    ..Actin and myosin filaments are organized in sarcomeres and specialized for producing contractile forces...
  41. Frisso G, Limongelli G, Pacileo G, Del Giudice A, Forgione L, Calabro P, et al. A child cohort study from southern Italy enlarges the genetic spectrum of hypertrophic cardiomyopathy. Clin Genet. 2009;76:91-101 pubmed publisher
  42. Rui Y, Bai J, Perrimon N. Sarcomere formation occurs by the assembly of multiple latent protein complexes. PLoS Genet. 2010;6:e1001208 pubmed publisher
    ..biochemically and are conserved across the animal kingdom, the mechanisms leading to the precise assembly of sarcomeres, the basic units of myofibrils, are poorly understood...
  43. Kowalski W, Gizak A, Rakus D. Phosphoglycerate mutase in mammalian striated muscles: subcellular localization and binding partners. FEBS Lett. 2009;583:1841-5 pubmed publisher
    ..It might suggest that PGM is a central structural element of the muscle glycolytic complex located within the isotropic region of the sarcomere. ..
  44. Garcia Castro M, Coto E, Reguero J, Berrazueta J, Alvarez V, Alonso B, et al. [Mutations in sarcomeric genes MYH7, MYBPC3, TNNT2, TNNI3, and TPM1 in patients with hypertrophic cardiomyopathy]. Rev Esp Cardiol. 2009;62:48-56 pubmed
    ..No phenotypic differences were observed between carriers of the various mutations, which makes it difficult to use genetic information to stratify risk in these patients. ..
  45. Chandra M, Mamidi R, Ford S, Hidalgo C, Witt C, Ottenheijm C, et al. Nebulin alters cross-bridge cycling kinetics and increases thin filament activation: a novel mechanism for increasing tension and reducing tension cost. J Biol Chem. 2009;284:30889-96 pubmed publisher
    ..These novel properties of nebulin add a new level of understanding of skeletal muscle function and provide a mechanism for the severe muscle weakness in patients with nebulin-based nemaline myopathy. ..
  46. Luther P. The vertebrate muscle Z-disc: sarcomere anchor for structure and signalling. J Muscle Res Cell Motil. 2009;30:171-85 pubmed publisher
    ..At the Z-disc the barbed ends of the antiparallel actin filaments from adjoining sarcomeres interdigitate and are crosslinked primarily by layers of alpha-actinin...
  47. de Tombe P, Mateja R, Tachampa K, Ait Mou Y, Farman G, Irving T. Myofilament length dependent activation. J Mol Cell Cardiol. 2010;48:851-8 pubmed publisher
  48. Gueneau L, Bertrand A, Jais J, Salih M, Stojkovic T, Wehnert M, et al. Mutations of the FHL1 gene cause Emery-Dreifuss muscular dystrophy. Am J Hum Genet. 2009;85:338-53 pubmed publisher
    ..In conclusion, FHL1 should be considered as a gene associated with the X-linked EDMD phenotype, as well as with hypertrophic cardiomyopathy. ..
  49. Pavlov I, Novinger R, Rassier D. The mechanical behavior of individual sarcomeres of myofibrils isolated from rabbit psoas muscle. Am J Physiol Cell Physiol. 2009;297:C1211-9 pubmed publisher
    The goal of this study was to develop a system to experiment with sarcomeres mechanically isolated from skeletal muscles...
  50. Ehler E, Gautel M. The sarcomere and sarcomerogenesis. Adv Exp Med Biol. 2008;642:1-14 pubmed
    ..appearance, caused by the longitudinal alignment of thousands of highly ordered contractile units, the sarcomeres. The assembly (and disassembly) of these multiprotein complexes (sarcomere assembly or sarcomerogenesis) follows ..
  51. Sato K, Ohtaki M, Shimamoto Y, Ishiwata S. A theory on auto-oscillation and contraction in striated muscle. Prog Biophys Mol Biol. 2011;105:199-207 pubmed publisher
    ..Thus, the present theory comprehensively explains the characteristics of auto-oscillation and contraction in the contractile system of striated muscle. ..
  52. Rice R, Guinto P, Dowell Martino C, He H, Hoyer K, Krenz M, et al. Cardiac myosin heavy chain isoform exchange alters the phenotype of cTnT-related cardiomyopathies in mouse hearts. J Mol Cell Cardiol. 2010;48:979-88 pubmed publisher
  53. Stoecker U, Telley I, Stussi E, Denoth J. A multisegmental cross-bridge kinetics model of the myofibril. J Theor Biol. 2009;259:714-26 pubmed publisher
    ..In one single myofibril thousands of sarcomeres are lined up as a series of linear motors...
  54. Hoskins A, Jacques A, Bardswell S, McKenna W, Tsang V, dos Remedios C, et al. Normal passive viscoelasticity but abnormal myofibrillar force generation in human hypertrophic cardiomyopathy. J Mol Cell Cardiol. 2010;49:737-45 pubmed publisher
    ..However, the low maximum Ca(2+)-activated force and high Ca(2+) sensitivity of the myofilaments are likely to contribute substantially to any systolic and diastolic dysfunction, respectively, in hearts of HCM patients...
  55. McNally E, Dellefave L. Sarcomere mutations in cardiogenesis and ventricular noncompaction. Trends Cardiovasc Med. 2009;19:17-21 pubmed publisher
    ..These human genetic findings support that normal myocardial and sarcomere function are required for proper compaction and septation and that these mutations also portend a high risk of developing heart failure in later life...
  56. Sawyer D, Peng X, Chen B, Pentassuglia L, Lim C. Mechanisms of anthracycline cardiac injury: can we identify strategies for cardioprotection?. Prog Cardiovasc Dis. 2010;53:105-13 pubmed publisher
    ..Moreover, assessing an individual's risk for anthracycline injury may be improved by having some measure of endogenous activity of this and other myocardial protective signals...
  57. Chung C, Granzier H. Contribution of titin and extracellular matrix to passive pressure and measurement of sarcomere length in the mouse left ventricle. J Mol Cell Cardiol. 2011;50:731-9 pubmed publisher
    ..2 ?m. In conclusion, within physiological volumes, titin is the dominant contributor to LV passive pressure, and ECM-based pressures dominate at larger volumes...
  58. Cuello F, Bardswell S, Haworth R, Ehler E, Sadayappan S, Kentish J, et al. Novel role for p90 ribosomal S6 kinase in the regulation of cardiac myofilament phosphorylation. J Biol Chem. 2011;286:5300-10 pubmed publisher
    ..We conclude that Ser(282) in cMyBP-C is a novel cardiac RSK substrate and its selective phosphorylation appears to regulate cardiac myofilament function...
  59. Câmara Pereira E, Campos L, Vannier Santos M, Mermelstein C, Costa M. Distribution of cytoskeletal and adhesion proteins in adult zebrafish skeletal muscle. Histol Histopathol. 2009;24:187-96 pubmed publisher
    ..Electron microscopical analysis in ultra-thin sections of adult zebrafish skeletal muscle showed bundles of collagen fibers and fibroblastic cells in the extracellular space of the myosepta...
  60. Janssen P. Myocardial contraction-relaxation coupling. Am J Physiol Heart Circ Physiol. 2010;299:H1741-9 pubmed publisher
  61. Meissner B, Warner A, Wong K, Dube N, Lorch A, McKay S, et al. An integrated strategy to study muscle development and myofilament structure in Caenorhabditis elegans. PLoS Genet. 2009;5:e1000537 pubmed publisher
    ..Many of the genes affecting sarcomere integrity have human homologs for which little or nothing is known...
  62. Shimamoto Y, Suzuki M, Mikhailenko S, Yasuda K, Ishiwata S. Inter-sarcomere coordination in muscle revealed through individual sarcomere response to quick stretch. Proc Natl Acad Sci U S A. 2009;106:11954-9 pubmed publisher
    The force generation and motion of muscle are produced by the collective work of thousands of sarcomeres, the basic structural units of striated muscle...
  63. Perkins A, Ellis S, Asghari P, Shamsian A, Moore E, Tanentzapf G. Integrin-mediated adhesion maintains sarcomeric integrity. Dev Biol. 2010;338:15-27 pubmed publisher
    ..Our results show that integrin-mediated adhesion is essential for maintaining sarcomeric integrity and illustrate that the seemingly stable adhesive contacts underlying sarcomeric architecture are inherently dynamic...
  64. Zhang R, Yang J, Zhu J, Xu X. Depletion of zebrafish Tcap leads to muscular dystrophy via disrupting sarcomere-membrane interaction, not sarcomere assembly. Hum Mol Genet. 2009;18:4130-40 pubmed publisher
    ..In addition, our data prompted a novel hypothesis that predicts that the transcription level of Tcap can be regulated by the stretch force to ensure proper sarcomere-membrane interaction in striated muscles...
  65. Leonard T, Herzog W. Regulation of muscle force in the absence of actin-myosin-based cross-bridge interaction. Am J Physiol Cell Physiol. 2010;299:C14-20 pubmed publisher
    ..These results suggest a mechanism for stability of sarcomeres on the "inherently unstable" descending limb of the force-length relationship, and they further ..
  66. Kimura A. Molecular basis of hereditary cardiomyopathy: abnormalities in calcium sensitivity, stretch response, stress response and beyond. J Hum Genet. 2010;55:81-90 pubmed publisher
  67. Campbell K. Interactions between connected half-sarcomeres produce emergent mechanical behavior in a mathematical model of muscle. PLoS Comput Biol. 2009;5:e1000560 pubmed publisher
    ..that attributes the stretch response of a mammalian fiber to the composite behavior of a collection of half-sarcomeres. The principal finding was that the stretch response of a chemically permeabilized rabbit psoas fiber could be ..