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Plk1 and Aurora A are activated through phosphorylation within their respective activation loops (T210 in human Plk1, T288 in human Aurora A; Jang et al. 2002; Littlepage et al. 2002), and both kinases are also controlled by additional mechanisms.
Contrasting motility modification due to OM with that from the natural myosin activator, specific βMys phosphorylation, provides insight into their respective activation mechanisms and indicates the boilerplate screening characteristics desired for pharmaceutical βMys activators.
Both CTL and antigen-presenting dendritic cells were activated as indicated by a decisive increase in their respective activation markers CD2, CD25, CD28 as well as CD48 and CD80.
Activation of the IKK complex in response to all stimuli is triggered by the phosphorylation of two key serine residues in their respective activation loops by the upstream kinase Tak1 [TGF (transforming growth factor -β-activated kinase 1] [ 15] In normal resting cells, cytosolic IκB binds and inhibits Nfactor -β-activateding to the nucleus factor -β-activatednscription.
Both reaction mechanisms exhibited relatively similar temperature dependencies, with respective activation energies of 56 and 68kJmol−1, determined between 25 and 45 °C, indicating reaction-controlled regimes.
Glass transition and crystallisation temperatures and their respective activation energies were determined; extrapolated onset values for these parameters have been determined in order to optimise the sintering temperature for producing amorphous coatings.
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However, respective activations of the regions belonging to these networks remain unknown with respect to chronometrical data when static drawing stimuli are presented.
In order to identify dominant stimulation pathways for each signalling protein, we assume that pathways with no affection on a protein do not significantly contribute to the respective activations (phosphorylation response).
With these values, we calculated the "specificity constant" as the ratio between the respective net activation fold over A0.5.
We attribute this to the recruitment of TLX to both MMP-2 and Oct-4 gene promoters, which resulted in the respective gene activation.
We presented happy and sad emotion expressions in increasing intensities from neutral (0%) through mild (50%) to intense (100%) to DPD and non-referred NC subjects in an implicit event-related fMRI design, and correlated respective brain activations with responses on the 20-item Toronto Alexithymia Scale (TAS-20) and its three subscales F1-F3.
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