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Pro-caspase-11 is inducible upon stimulation of multiple ligands involved in innate immunity, including LPS, IFNγ, and type I IFN (Broz et al., 2012; Gurung et al., 2012; Hur et al., 2001; Lee et al., 2001; Lin et al., 2000; Rathinam et al., 2012; Schauvliege et al., 2002; Wang et al., 1998; Yen and Ganea, 2009).
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Potential for development of multiple ligands for dopamine receptors involved in numerous neurological disorders was comprehensively reported by Butini et al. [61].
Chronic inflammatory diseases usually involve multiple ligands that act synergistically through promiscuous and diverse receptors1.
Chronic inflammatory diseases usually involve multiple ligands and receptors acting in concert.
For more complicated reaction schemes involving multiple ligands, multi-subunit enzymes and other complications the resulting kinetic laws are more complex but still can be derived following the standard procedures if the reaction mechanism is known and mass-action kinetics is assumed.
These P450s appear to have more complex, multiphasic kinetics, and movement to the proximity of the iron is a slower, more complex process, which in some of the cases involves multiple ligands being present.
The major ligand involved in TLR4 activation is endotoxin [ 5].
Furthermore, depending on T cell type and T cell stimulus, direct cellular contact with stimulated T lymphocytes can induce different patterns of products in monocytes/macrophages (reviewed in [3], [4], [11]), suggesting that multiple ligands and counter-ligands are involved in the contact-mediated activation of monocytes/macrophages.
This suggests that multiple ligands and counter-ligands are involved in the contact-mediated activation of monocytes/macrophages that are differentially induced on T cells (depending on the stimulus) and differentially induce monocyte/macrophage signal transduction.
However, the synthesis of ligand involves multiple steps.
To support our general theory we consider two reaction schemes involving the binding of multiple ligands (substrates and inhibitors) to the free enzyme (Fig. 1b and c).
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