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This suggests that ACh release, even if unable to evoke functional electrophysiological responses, contributes to regulating the appearance of new AChR-rich sites on growing myofibers.
However, relative differences in DA tissue content among the four regions (Fig. 1a) were not matched by TH content in these tissues (Fig. 1b) [note that actual values are indicated in figure legend to support this finding], signifying that site-specific phosphorylation also contributes to regulating inherent DA tissue content in the CNS.
Constitutive degradation of the Met receptor by PS-RIP contributes to regulating its half-life.
Thus the GADD45beta gene also contributes to regulating the cell cycle.
Conversely, these results are consistent with the notion that sAC contributes to regulating basal levels of cAMP.
These results suggest that Neurod contributes to regulating the expression of some phototransduction genes, both in rod and cone photoreceptors.
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Moreover, PPAR gamma contributes to regulate some key circadian genes.
Here we reveal that SMG1C (a complex containing SMG1, SMG8, and SMG9) contributes to regulate NMD by recruiting UPF1 and UPF2 to distinct sites in the vicinity of the kinase domain.
Functionally, mobility of neurotransmitter receptors contributes to regulate synaptic function by multiple mechanisms.
Direct administration of leptin into the hippocampus in mice improves memory processing and increases the expression of NMDA receptors, enhances learning and memory performance, and contributes to regulate hippocampal synaptic plasticity [33].
Although the activity of PDE2 toward the hydrolysis of cAMP is relatively low, its presence in plasma membrane contributes to regulate the cardiac LTCC activity when the level of cGMP is increased [44], since PDE2 inhibits the activation of LTCCs by reducing cAMP concentration after being activated by cGMP.
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