Consistent with our results, a previous study (using the same line of mice with loxP-flanked Hb-egf cDNA) demonstrated that a mutation of the Hb-egf gene was associated with decreases in the activation of EGF receptor and ERK [49].
In vitro, G28UCM showed marked synergistic interactions with trastuzumab, lapatinib, erlotinib or gefitinib (but not with cetuximab), which correlated with increases in apoptosis and with decreases in the activation of HER2, extracellular signal-regulated kinase (ERK 1/2 and AKT.
In conclusion, CGRP significantly inhibits angiotensin II-induced proliferation of vascular smooth muscle cells, an effect related to a decrease in the activation of mitogen-activated protein kinase pathway.
Finally, exogenous nucleosides also rescue RP-deficient zebrafish by resulting in the downregulation of pro-apoptotic p53 targets and a decrease in the activation of AMP-activated protein kinase.
As interference with the SH2-kinase domain interface leads to a dramatic reduction in Bcr-Abl activity, one would expect a uniform decrease in the activation of the major pathways that are activated by Bcr-Abl.
These events coincided with a decrease in the activation of Akt via pThr308, the appearance of active pThr286 CaMKII and subsequent reduction of nNOS activity via an increase of pSer847 and dephosphorylation of pSer1417.
In other clinical studies in patients with sepsis, mainly caused by pulmonary sources, investigators found a drastic decrease in the activation of chemokines, neutrophils and vascular endothelial cells with PMX-HP [13, 35], as a result pulmonary function improved.
One way in which neuron populations may experience this transition could be a decrease in the activation of dampening, shortly after entering the bursting mode.
A previous report [44] suggested that loss of Grb2 in T cells results in a decrease in the activation of Jnk, but not extracellular signal-regulated kinase (ERK), and our data confirm this: the synergy between Grb2 and Dvl2 is blocked by the Jnk inhibitor SP600125, and by the dominant negative c-jun, junAA (Fig. 5), but not by an ERK inhibitor or by dominant negative Ras (data not shown).
This slight decrease in the total excitation with the frequency explains the slight decrease in the activation of GC when inhibition was blocked.
In contrast, T-DNA knockout or transcription repressor plant lines show a marked decrease in the activation of these defense-associated genes.
