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C3b enhances opsonisation by binding to both phagocytes and pathogens [ 12].
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HGF treatment inhibited binding to both.
Antibody-targeted therapeutics are known to provide imperfect tumor targeting, and show uptake in liver and spleen via Fc-mediated binding to phagocytes.
After binding to these opsonins, phagocytes engulf pathogens or damaged cells, and eliminate them through the generation of reactive oxygen species and hydrolytic enzymes.
On binding to these signals, phagocytes upregulate the expression of specific genes involved in phagocytosis, such as MFG-E8, a bridging molecule that recognises phosphatidyl serine (an 'eat-me' signal) on the apoptotic cell and integrins on the phagocyte.
RB or POS tips, that are respectively detached from either living nonapoptotic germ cells or from photoreceptor cells, are phosphatidylserine (PS -exposing membranes as evidenced by their strong binding to ANXA5/annexin A5., The PS -exposingrocess involves substrate binding, ingestion and degradation by phagocytes.
NBD and Anxa5-GPI double-positive cells were considered as phagocytes binding to lipid vesicles.
This parasite-leukocyte ratio allowed for a high parasite burden and a low level of phagocyte binding to the connective tissue or to isolated connective matrix components in adhesion assays [ 12].
sIgA can also act as opsonin, signaling the presence of antigens to phagocytes by binding to the surface of bacteria and facilitating aggregation.
M-CSF selectively regulates the growth and survival of mononuclear phagocytes by binding to a specific cell surface receptor, c-fms.
CD14 is located at the exofacial leaflet of the plasma membrane through its GPI anchor, which rules out the possibility that it mediates direct signal transduction into phagocytes after binding to apoptotic cells.
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