Consequently, the two stimuli, 8Br-cAMP and EGF, favor scenarios of pERK distribution –localization in the mitochondria and steroidogenesis or in the nucleus and cell proliferation, respectively - that are qualitatively and quantitatively rather different.
Although the ratio N/C for ERK was constant in P1 and P10, significant differences were detected with respect to pERK distribution.
To determine the subsynaptic distribution of pERK in dendritic spine profiles, we divided the spine head profile into three distinct compartments: post-synaptic density (PSD), shell and core [19].
To assess the temporal dynamics of ERK activation at synaptic sites, we investigated the distribution of pERK immunogold labelling at different times after visual stimulation (2.5, 15, and 40 min).
For the calculation of pathway bias, the pAKT response was linearly scaled by a factor of 2.386 to minimize the Cramér-Von Mises distance between the distribution of pERK and pAKT fold-change responses.
However, in both treatments the characteristic asymmetric dorsoventral distribution of pErk positive cells (Figs 4H, 6A) is disrupted and these cells are evenly distributed throughout the animal ectoderm (Fig. 6B,E).
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However, after optic nerve injury, the distribution of pERK-1 changed dramatically.
From this analysis, we conclude that RSK is not only required for regulation of pERK levels, but also determines the distribution of pERK within different motoneuron compartments.
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Analyses on the distribution and mRNA expression levels of grp78, crt, perk, eif2α, ire-1α, xbp-1, and atf-6α were conducted by quantitative real-time PCR (qPCR) method.
