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Here, both infectious forms of VACV, mature virion (MV) and enveloped virion (EV), induce their own macropinocytosis by binding to the cell surface and triggering an actin-mediated plasma membrane protrusion that eventually collapses back onto the plasma membrane sealing the attached virion inside a macropinosome, which then goes through a ...
Pinocytosis. In cellular biology, pinocytosis, otherwise known as fluid endocytosis and bulk-phase pinocytosis, is a mode of endocytosis in which small molecules dissolved in extracellular fluid are brought into the cell through an invagination of the cell membrane, resulting in their containment within a small vesicle inside the cell.
Actin is a family of globular multi-functional proteins that form microfilaments in the cytoskeleton, and the thin filaments in muscle fibrils.It is found in essentially all eukaryotic cells, where it may be present at a concentration of over 100 μM; its mass is roughly 42 kDa, with a diameter of 4 to 7 nm.
This releases tropomyosin, exposing active sites of the thin filament, actin. There are several mechanisms directly linked to the terminal cisternae which facilitate excitation-contraction coupling. When excitation of the membrane arrives at the T-tubule nearest the muscle fiber, a dihydropyridine channel (DHP channel) is activated. [2]
Actin, cytoplasmic 2, or gamma-actin is a protein that in humans is encoded by the ACTG1 gene. [5] Gamma-actin is widely expressed in cellular cytoskeletons of many tissues; in adult striated muscle cells, gamma-actin is localized to Z-discs and costamere structures, which are responsible for force transduction and transmission in muscle cells.
Bleb growth is driven by intracellular pressure (abnormal growth) generated in the cytoplasm when the actin cortex undergoes actomyosin contractions. [5] The disruption of the membrane-actin cortex interactions [4] are dependent on the activity of myosin-ATPase [6] Bleb initiation is affected by three main factors: high intracellular pressure, decreased amounts of cortex-membrane linker ...
Because actin monomers must be recycled to sustain high rates of actin-based motility during chemotaxis, cell signalling is believed to activate cofilin, the actin-filament depolymerizing protein which binds to ADP-rich actin subunits nearest the filament's pointed-end and promotes filament fragmentation, with concomitant depolymerization in ...
The unfavorable kinetics of actin oligomer production prevent spontaneous actin polymerization. [2] Once an actin nucleus has been created, the connection of the monomers happens swiftly, with the plus end developing considerably more quickly than the minus end. [2] Actin's ATPase activity sharply rises after insertion into the filament. [2]