contractile filament

Several models of contractile filament architecture are discussed here.

The freezing process was associated with a phase transition in the interstices between the contractile filaments.

When myosin is activated, the contractile filaments slide apart and the muscle cell relaxes.

This may be considered as indirect evidence that the conductivity of the contractile filaments is associated with the protein counter-ions, since Hinke et al.

Imagine a hollow tube made up of a layer of cells just one cell thick with contractile filaments located near the outer surface.

This was interpreted as evidence that the counterions around the contractile filaments occupied a nonnegligible fraction of the intracellular compartment.

They possess rudimentary contractile filaments, but contract relatively weakly compared to the cardiac contractile cells.

The cytoskeleton is represented as a 2-D network of links (contractile filaments) connecting nodes (adhesion plaques).

Smooth muscle plasticity is a mechanism likely implicated in asthma, whereby contractile filament rearrangements lead to maximal force production, independent of muscle length.

Muscle is formed of contractile filaments and is separated into three main types; smooth muscle, skeletal muscle and cardiac muscle.

The putative mechanism of initiation of the propagating Ca2+ waves involves feedback of rapid length (or force) changes to dissociation of Ca2+ from the contractile filaments.

SA node fibres are specialized cardiomyocytes that vaguely resemble normal, contractile cardiac myocytes; however, although they possess some contractile filaments they do not contract as robustly.

We interpret this excess Na to be a measure of the amount of myoplasmic Na which is acting as counterion for the fixed negative charge on the contractile filaments.

There is evidence that the myofilament lattice in some smooth muscles, such as airway smooth muscle, is malleable; it can be reshaped to fit a large range of cell dimensions while the maximal overlap between the contractile filaments is maintained.

This delayed onset muscle soreness (DOMS) results from structural damage to the contractile filaments and z-disks, which has been noted especially in marathon runners whose muscle fibers revealed remarkable damage to the muscle fibers after both training and marathon competition .

It is believed that the contractile filaments in smooth muscle are organized into arrays of contractile units (similar to the sarcomeric structure in striated muscle), and that such an organization is crucial for transforming the mechanical activities of actomyosin interaction into cell shortening and force generation.