In response to a lack of nutrients, p53 becomes activated through the activation of AMP-activated protein kinase (AMPK) and the inhibition of AKT.
However, in disease states, GSK-3β becomes activated through the elimination of inactivation signals, leading to neurodegeneration.
The construction of toxins that become activated through cleavage by the protease (HIV-1 PR) expressed by the HIV-1 virus is described.
The variety of the detected phosphoproteins indicated that signaling pathways from the plasma membrane to the nucleus become activated through phosphorylation events.
It is now known that the MHC makeup on the surface of those cells is altered and the NK cells become activated through recognition of "missing self".
The involvement of T cells in the FBR to nonphagocytosable implants has not been fully elucidated; however T cells have been shown to attach to the biomaterial [ 92] and become activated through noncanonical pathways [ 93– 96], as well as enhancing macrophage adhesion and fusion into FBGCs through paracrine actions of secreted cytokines [ 97– 97].
Upstream initiator Caspases become activated through protein interactions involving assembly of multi-protein complexes (reviewed in [2], [3]), which are often difficult to reconstitute in vitro.
When RAS family members become activated, through physiological stimuli or through mutation [7], [17], [42], [43], they signal to key pathways involved in cell growth, survival, differentiation and migration, including the RAF-MAPK [44], PI3K [45], and the RALGEF (RALGDS; ral guanine-nucleotide-dissociation stimulator) [46] pathways.
During acute inflammation, M1 macrophages become activated through a classical pathway and are able to kill and phagocytose tumour cells.
