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Sialic acid binding is shown to trigger a conformational switch that modulates the affinity for the acceptor substrate and concomitantly creates the conditions for efficient transglycosylation.
Such difference in the intensity of stress is shown to trigger different response even in the case of other stress responses such as in osmotic stress, where cells survived severe osmotic stress by accumulating trehalose and moderate osmotic stress through glycerol accumulation [46], [47].
Wnt signalling is shown to trigger the sequestration of GSK3 from the cytosol into multivesicular bodies (MVBs) so that the enzyme becomes separated from its cytosolic substrates.
Moreover, Ang II receptors, AT1 and AT2, have been widely investigated as intermediates for pathological stimuli in the cardiovascular system, where the stimulation of AT1 (a G-protein-coupling receptor) is shown to trigger vasoconstriction signalling [ 62, 67] and cardiac hypertrophy through the activation of mitogen-activated protein kinase (MAPK) and protein kinase (PK) [ 68].
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Such focused interventions have been shown to trigger far-reaching positive consequences (Aguilar et al. 2014).
It has also previously been shown to trigger the release of chemicals in the brain that might facilitate bonding.
In several nanosafety studies, exposure to nTiO2 has been shown to trigger inflammation in mice lung and to cause oxidative stress.
NO donors such as GTN have been shown to trigger an early onset headache and migraine attack in sufferers after a delay of hours [26, 42].
However, SCARB2 has been shown to trigger the uncoating process of EV71 in an acidic environment (Chen et al., 2012; Yamayoshi et al., 2013).
Indeed, for pathogenic bacteria T3Es were shown to trigger and to subvert host defences.
DZNep has been shown to trigger proteasomal degradation of PRC2 components [14].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com