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CCL2 has been shown to increase HIV-1 entry into resting CD4+ T cells [41] and trigger recruitment of HIV-1-susceptible target cells [42].
Therefore, it is possible that expression of Shank1b may trigger recruitment and morphological changes of presynaptic complexes and this process may be critical for stabilization of dendritic filopodia.
In our previous studies, we found that the transformed cells trigger recruitment of several innate immune cell lineages [ 14].
Rac1 and Basket/JNK signaling have also been previously implicated in hemocyte activation [ 63] and therefore represent potential downstream targets of signaling pathways to trigger recruitment of hemocytes from the circulation.
This suggests that TE fragments could act as facilitators of DNA methylation recruitment [ 66]: presence of TE fragments would trigger recruitment of the RdDM machinery in control conditions, and this pathway would be even more active following cold conditions.
We show that relatively large or chronic wounds trigger recruitment of pigment cell lineages in both larvae and adults, which leads to hyperpigmentation, and that this process is associated with, and dependent on, the preceding inflammatory events.
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IpaD [Ipa (invasion plasmid antigen)] is the first protein to localize to the T3SA needle tip, where it prevents premature effector secretion and serves as an environmental sensor for triggering recruitment of the translocator protein IpaB to the needle tip.
Furthermore, CCL2 may increase HIV-1 entry into resting CD4+ T cells [41] and triggers recruitment of HIV-1-susceptible target cells [42].
To assess whether phosphorylation of Atg9 triggers recruitment of these proteins, we analyzed their PAS localization.
Activation of death receptors triggers recruitment of FADD and subsequent processing of caspase-8.
NPF recruitment and their activation were separable, as SopE triggered recruitment of N-WASP and WRC but only N-WASP was activated.
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