Ravid and coworkers [ 20] have shown that activation of A2AR increases A3AR promoter activity.
It has been shown that activation of MAPKs can phosphorylate and activate a number of signaling pathways, including p53.
Some studies have shown that activation of MAPK phosphorylation transduction signals could activate downstream transcription of NF-κB-mediated pro-inflammatory cytokines.
For example, it has been shown that activation of ERK1/2, through the Raf-mediated Ras pathway, increases the activity of HIF1 and Sp1 transcription factors [ 20, 33].
It is shown that activation of the pac gene transcription is elevated by IHF.
Animal studies have shown that activation of the cannabinoid system during extinction learning enhances fear extinction and its retention.
Experimental studies have shown that activation of bradykinin B2 receptor is one of the most important triggers of ischemic preconditioning.
It has been shown that activation of glia contributes to the development of behavioral hypersensitivity after peripheral inflammation.
It has been shown that activation of c-Abl by many sources of DNA damage is associated with inhibition of cell growth and induction of apoptosis (Kharbanda et al., 1998; Wang, 2000).
In experimental settings, it has been shown that activation of caspase-3 resulted in significant ROS production.
Previous studies have shown that activation of pSTAT-3 is required for expression of Bcl-xL [34].
