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| Open AccessHighly durable crack sensor integrated with silicone rubber cantilever for measuring cardiac contractility
Measuring cardiac contractility is challenging. Here, the authors encapsulated a crack-based sensor with polydimethylsiloxane, thereby endowing the sensor with the stability to measure cardiac contractility for up to 26 days as well as monitoring drug-induced cardiac toxicity in cell culture.
- Dong-Su Kim
- , Yong Whan Choi
- & Dong-Weon Lee
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Article
| Open AccessProtein phosphatase 5 regulates titin phosphorylation and function at a sarcomere-associated mechanosensor complex in cardiomyocytes
Protein phosphatase 5 (PP5) is expressed in many cell types but its role in cardiomyocytes is unknown. Here the authors show that PP5 binds and dephosphorylates elastic titin in cardiac sarcomeres, and that PP5 is increased in heart failure, reducing cardiomyocyte compliance.
- Judith Krysiak
- , Andreas Unger
- & Wolfgang A. Linke
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| Open AccessStructure of actomyosin rigour complex at 5.2 Å resolution and insights into the ATPase cycle mechanism
The cyclic association and dissociation of myosin with actin filament is regulated by ATP binding and hydrolysis cycles. Here the authors report the structure of mammalian skeletal muscle actomyosin rigour complex that provides insights into the ATPase-coupled reaction cycle of actomyosin.
- Takashi Fujii
- & Keiichi Namba
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| Open AccessThick filament mechano-sensing is a calcium-independent regulatory mechanism in skeletal muscle
Recent data suggest that muscle contraction is regulated by thick filament mechano-sensing in addition to the well-known thin filament-mediated calcium signalling pathway. Here the authors provide direct evidence that myosin activation in skeletal muscle is controlled by thick filament stress independently of calcium.
- L. Fusi
- , E. Brunello
- & M. Irving
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| Open AccessDirect optical activation of skeletal muscle fibres efficiently controls muscle contraction and attenuates denervation atrophy
Nerve damage can lead to skeletal muscle paralysis and atrophy. Here, the authors show that localized photostimulation of mouse calf muscle expressing the light-sensitive channel Channelrhodopsin-2 generates contraction in the absence of neural impulses and prove that this strategy can be used to prevent muscle atrophy.
- Philippe Magown
- , Basavaraj Shettar
- & Victor F. Rafuse
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Drebrin-like protein DBN-1 is a sarcomere component that stabilizes actin filaments during muscle contraction
Muscle function depends on a highly organized array of actin and myosin filaments. Butkevichet al. identify the C. elegansdrebrin-like protein DBN-1 as an important regulator of actin filament stability in muscle cells, which relocalises from M-lines to I-bands on contraction.
- Eugenia Butkevich
- , Kai Bodensiek
- & Dieter R. Klopfenstein
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Substrate stiffness-modulated registry phase correlations in cardiomyocytes map structural order to coherent beating
Cardiomyocyte function depends on the interplay between the intracellular fibrillar organization, contraction strain and substrate stiffness. Here the authors present a model that maps the measured values of the registry striations to those of the beating strain as functions of the substrate rigidity.
- K. Dasbiswas
- , S. Majkut
- & Samuel A. Safran
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Diminished hERG K+ channel activity facilitates strong human labour contractions but is dysregulated in obese women
Uterine muscle contracts rhythmically during labour but the underlying electrophysiological mechanisms are not fully understood. The authors of this study show that hERG1 potassium channels reduce human uterine contractions in pregnancy and are suppressed during labour in lean but not in obese women.
- Helena C. Parkington
- , Janet Stevenson
- & Roger Smith
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Enhanced dihydropyridine receptor calcium channel activity restores muscle strength in JP45/CASQ1 double knockout mice
Calcium influx through the Cav1.1 channel initiates skeletal muscle contractions. Zorzato and colleagues report a role for the proteins JP45 and calsequestrin in strengthening skeletal muscle contraction by modulating Cav1.1 channel activity.
- Barbara Mosca
- , Osvaldo Delbono
- & Francesco Zorzato