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These results demonstrate that in adulthood neuronally derived d-serine, which is required for optimal activation of post-synaptic NMDAR activity, regulates pyramidal neuron dendritic arborization and spine density.

That either the S65A ubiquitin mutant or the Parkin S65A mutant alone can substantially reduce, but not abolish, Parkin E3 ligase activity indicates that both PINK1-dependent phosphorylation of Parkin at Ser and ubiquitin at Ser are required for mediating optimal activation of Parkin E3 ligase activity.

Recently, we described that the Vav1 and RasGRF2 GEFs play synergistic roles in the activation of specific T cell receptor (TCR) downstream signaling pathways, including the optimal activation of phospholipase C γ, the stimulation of the nuclear factor of activated T cells, and the transcriptional upregulation of cytokine genes [18].

Our biochemical analyses revealed that LRRK2 was required for optimal activation of Rip2, TAK1, NF-κB and MAPKs.

Different models have been proposed to understand which parameters are needed to obtain an optimal activation of the signaling.

The oligosaccharides at Asn297 of the IgG-Fc are essential for the optimal activation of FcγRs and complement C1 although the carbohydrate moiety accounts for only 2%3%% of the IgG molecule.

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In contrast, sub-optimal activation of macrophages and induction of a dysregulated host cell lipid metabolism favored a less stressful intracellular environment for HN878.

Whereas the early and highly activated BMM induced by CDC1551 infection triggered a rapid and robust Mtb stress response, the sub-optimal activation of BMM upon infection by HN878 resulted in diminished environmental pressure on the bacteria [ 19, 21].

HN878 infection is associated with lung inflammation, followed by a slow and sub-optimal activation of the host innate and adaptive immune responses and the sustained presence of activated CD4+ and CD8+ T cells throughout the course of infection, which seems to be driven by the bacillary load in the lungs [ 12].

Optimal activation of NF-κB requires the phosphorylation of p65.

Optimal activation of NF-κB requires phosphorylation (e.g. serine phosphorylation) in the transactivation domain of p65.

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