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First, allosteric modulators can affect one receptor by binding to another receptor within a dimeric or oligomeric complex.
In the context of platelet membranes, THBS1 promotes thrombosis in at least two ways: (1) it stimulates platelet aggregation through CD36 receptor-based inhibition of kinase signaling cascades [ 54], and (2) THBS1 acutely counteracts the promotion of blood flow by nitric oxide via binding to another receptor, CD47, on vascular smooth muscle cells [ 55, 56].
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MIF binds to cell-surface CD74 [15] and the MIF-CD74 complex then activates signal transduction by binding to another cell-surface receptor, CD44 [14].
NCAM is a membrane glycoprotein receptor of the immunoglobulin supergene family that mediates cell-to-cell adhesion via homophilic binding to other NCAM molecules and cell-to-substrate adhesion via heterophilic binding (NCAM binding to another ligand or counter-receptor) [ 30].
Indeed, a neutralizing anti-IL-8 antibody has significantly reduced ischemia-induced brain damage [66], further suggesting that inhibition of IL-8 binding to its receptor CXCR1 is another potential target for inhibiting the IL-8 effects [68], and the decreased CXCR1 expression may play a neuroprotective role.
Another approach to reverse LecA binding to its receptor is to utilise the calcium chelator ethylenediaminetetraacetic acid (EDTA).
After binding to a receptor, an antagonist can block the effect of an agonist.
Chemicals that block nicotine's binding to the receptor also blocked proliferation of the cells.
We began with the simplest act of a molecule binding to its receptor.
A competitive binding inhibitor of TLR4 blocked AGE-LDL binding to the receptor.
AGE perfusion-induced LTP reduction may be caused by varying factors; for example, one cause involves AGE binding to RAGE receptors, and another is via protein crosslinking-induced cellular malfunction.
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