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It has been reported that activation of canonical Wnt signaling may bring out opposite biological activity in the context of osteogenic differentiation depending on the threshold levels of its activation, the status of cell, and Wnt ligands concentration [ 24].
In several publications, it has been reported that activation of the default mode network (DMN) can be reduced or altered in different neuropsychiatric and neurological disorders in adults.
It has been reported that activation of AKT blocks conformational change of Bax as well as its translocation to mitochondria under stress stimuli [24].
It has been reported that activation function 1 (AF1) domain of ERα binds to α- and β-tubulins in MCF-7 breast carcinoma cells [14].
Concerning angiogenesis, it has been reported that activation of Shh cascade evoked in vitro capillary-like structures formation and in vivo new blood vessel generation [10] [12].
It has been reported that activation of FOXO transcription factors induces Bim mRNA expression and promotes cell apoptosis in a Bim-dependent manner [19], [20].
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In recent works it was reported that activation of Vegf/Vegfr2 and Angiopoietin/Tie2 signalling is modulated by BMP (bone morphogenetic protein) signaling-activation in endothelium [177].
It was reported that activation of GSK3 β could be regulated by multiple factors.
It was reported that activation of p38 MAPK, AKT1, and NF- κB in neutrophils contributes to ALI [ 85].
It is reported that activation of P2Y2 receptor can lead to an increase in cell growth in most types of cancer such as melanoma and lung tumours (Schafer et al, 2003; White et al, 2005).
It was reported that activation of the NF-κB dependent genes occurs with no delays after NF-κB enters the nucleus, whereas IRF3 enters nucleus before NF-κB, but its nuclear translocation profile suggests presence of additional modifying factors, which delay IRF3-mediated activation [ 28].
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