Information om | Engelska ordet MYOFIBRILS

Exempel på hur man kan använda MYOFIBRILS i en mening

• Skeletal muscle, is a type of striated muscle, composed of muscle cells, called muscle fibers, which are in turn composed of myofibrils.
• The myofibrils are composed of actin and myosin filaments called myofilaments, repeated in units called sarcomeres, which are the basic functional, contractile units of the muscle fiber necessary for muscle contraction.
• Skeletal muscle cells and cardiac muscle cells both contain myofibrils and sarcomeres and form a striated muscle tissue.
• The stretching sarcomeres augments cardiac muscle contraction by increasing the calcium sensitivity of the myofibrils, causing a greater number of actin-myosin cross-bridges to form within the muscle.
• A study performed by Magid and Law demonstrated that the origin of passive muscle tension (which occurs during stretching) is actually within the myofibrils, not extracellularly as had previously been supposed.
• In adult desmin-null mice, hearts from 10 week-old animals showed drastic alterations in muscle architecture, including a misalignment of myofibrils and disorganization and swelling of mitochondria; findings that were more severe in cardiac relative to skeletal muscle.
• Postnatal sarcomere disorganization and degeneration occurred rapidly in these mice, indicating the nebulin is essential for maintaining the structural integrity of myofibrils.
• In colliquative myocytolysis, fluids accumulated within the cell dissolve myofibrils, resulting in vacuolization of the cell.
• Costameres are sub-sarcolemmal protein assemblies circumferentially aligned in register with the Z-disk of peripheral myofibrils.
• A myocyte is composed of multiple myofibrils, which contain the “contractile units” of the muscle known as a sarcomere.
• 5, coordinate with severe cardiac muscle abnormalities including left ventricular hyperplasia, sinuatrial valve abnormalities, pericardial edema, thoracic hemorrhaging, myocardial wall degeneration, regional apoptosis, reduced density and disorganization of myofibrils, and enlarged mitochondria.
• S100A1 overexpression via adenoviral gene transfer in adult rabbit cardiomyocytes or a cardiac-restricted S100A1 murine transgenic enhanced cardiac contractile performance by increasing sarcoplasmic reticular calcium transients and uptake, altering the calcium sensitivity and cooperativity of myofibrils, enhancing SERCA2A activity and enhancing calcium-induced calcium release.
• Treating cardiac myofibrils with the lysine-rich N-terminal peptide (amino acids 5-14) evoked a supramaximal increase in cardiac myofibrillar MgATPase activity at submaximal calcium concentrations, and further studies demonstrated that this region of ELC modulates the affinity of myosin for actin.
• Obscurin is expressed in cardiac and skeletal muscle, and plays a role in the organization of myofibrils during sarcomere assembly.
• In muscle, the interaction of CapZ with actin is critical during myofibrilogenesis, as administration of a CapZ monoclonal antibody or expression of CapZ mutant protein disrupts actin filament formation and assembly of myofibrils.
• They are generally much smaller than the contractile cells and have few of the myofibrils or myofilaments which means that they have limited contractibility.
• Further observation of the myofibrils, and the crude preparations of the extracted contractile protein actins and myosins taken from them, showed that they required trace levels of calcium for contractile activity.
• A decreased availability of 250HD leads to mishandling of cellular calcium transport to the sarcoplasmic reticulum and mitochondria, and is associated with reduced actomyosin content of myofibrils.
• During his early years at UT, Wang and his co-workers discovered two previously unrecognized high molecular weight proteins of myofibrils, Titin and Nebulin, which fundamentally changed our understanding of muscle sarcomeres.

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