cytoplasmic vesicle

However, most will be found within the plasma membranes of cytoplasmic vesicles within the cell.

PrPSc is probably located within neuronal processes in cytoplasmic vesicles.

The nucleocapsids finally gain their secondary envelopes by budding into cytoplasmic vesicles within the cell.

These particles often cluster in between the inner and outer nuclear membranes, causing visible projections which often evaginate into cytoplasmic vesicles.

The main route of endocytosis is the coated pit, which buds into a cell to form a cytoplasmic vesicle - a clathrin-coated vesicle.

The encoded protein localizes to the nuclear matrix, PML nuclear bodies, and cytoplasmic vesicles.

A second type of reuptake inhibition affects vesicular transport, and blocks the intracellular repackaging of neurotransmitters into cytoplasmic vesicles.

Interactions from calcineurin activate dynamin GTPase activity, allowing the clathrin pit to excise itself from the cell membrane and become a cytoplasmic vesicle.

The free base form accumulates in lysosomes (acidic cytoplasmic vesicles) and is then protonated, resulting in concentrations within lysosomes up to 1000 times higher than in culture media.

Electron microscopy has revealed clusters of viral particles positioned perpendicular to the inner nuclear membrane, the endoplasmic reticulum, as well as the aforementioned cytoplasmic vesicles, forming distinctive "spoked wheel"

Yet another mechanism has been suggested for secretin induction of HCO 3 -uptake into bile ductular cells: insertion of cytoplasmic vesicles containing H + ATPase into the basolateral membrane.

The monocytes differentiate into macrophages, which ingest oxidized LDL, slowly turning into large "foam cells" - so-called because of their changed appearance resulting from the numerous internal cytoplasmic vesicles and resulting high lipid content.

After a meal and at the binding of insulin (released from the islets of Langerhans) to receptors on the cell surface, a signalling cascade begins which culminates in the movement of the cytoplasmic vesicles toward the cell surface membrane.

It is also unclear whether the increased apical membrane K + and Cl -permeabilities result from activation of latent transport systems or, alternatively, from insertion of a separate class of K + and Cl -permeable cytoplasmic vesicles into the apical membrane.

The poloxamers have also been shown to enhance proto-apoptotic signaling, decrease anti-apoptoic defense in MDR cells, inhibit the glutathione/glutathione S-transferase detoxification system, induce the release of cytochrome C, increase reactive oxygen species in the cytoplasm, and abolish drug sequestering within cytoplasmic vesicles.