लक्ष्य-प्रकोष्ठ इसके अंग्रेजी अर्थ का उदाहरण

The bacterial outer membrane is physiologically shed as the bounding membrane of outer membrane vesicles in cultures, as well as in animal tissues at the [interface], implicated in translocation of gram-negative microbial biochemical signals to host or target cells.

During ADCC, FcγRIII receptors on the surface of natural killer (NK) cells stimulate the NK cells to release cytotoxic molecules from their granules to kill antibody-covered target cells.

The Fc receptor on NK cells recognize IgG that is bound to the surface of a pathogen-infected target cell and is called CD16 or FcγRIII.

Activation of FcγRIII by IgG causes the release of cytokines such as IFN-γ that signal to other immune cells, and cytotoxic mediators like perforin and granzyme that enter the target cell and promote cell death by triggering apoptosis.

rhamnosus GR-1 utilises lectin-like proteins to attach to carbohydrates on the surface of the target cell.

Other properties attributed to the cytokine include: the growth promotion and cell differentiation of different types of target cells, influence on bone metabolism, cachexia, neural development, embryogenesis and inflammation.

RARs mediate transcription of different sets of genes controlling differentiation of a variety of cell types, thus the target genes regulated depend upon the target cells.

Activation of GABA receptors on these cells, whether they are ionotropic or metabotropic, typically results in the influx of chloride ions into that target cell.

This build-up of negative charge from the chloride ions results in the hyperpolarization of the target cell, making it less likely to fire an action potential.

Since this reduction of inhibitory currents could be invoked simply by depolarization of the target cell, this phenomenon was termed depolarization-induced suppression of inhibition.

Somehow, depolarization-induced suppression of inhibition appeared to be mediated by a retrograde synaptic messenger whose synthesis or release was stimulated by the depolarization of the target cell.

LTA may bind to target cells non-specifically through membrane phospholipids, or specifically to CD14 and to Toll-like receptors.

Although tetrameric pore formation of α-latrotoxin has been shown conclusively , some authors still dispute whether this is the main mode of action of α-latrotoxin, and believe that α-latrotoxin (tetrameric or not) may penetrate through the membrane of target cells to interact directly with intracellular neurotransmitter release machinery.