Among these caspases, caspases 8, 9, and 10 are initiator caspases that are activated through binding to specific proteins, while caspase-3 is an effector caspase that is subsequently activated by the active initiator caspases through proteolytic cleavage.
AR is activated through binding of a ligand, such as testosterone or DHT, to its ligand-binding domain (LBD), followed by dissociation of inhibitory heat-shock proteins.
In these cases, histamine signaling is induced by G protein coupled receptors, that are activated through binding histamine as non-covalent ligand [16,17].
Calcineurin is activated through binding of Ca2+/calmodulin (CaM) and then dephosphorylates the cytosolic form of Crz1/CrzA, which is then translocated to the nucleus for the activation of downstream targets (7, 9).
The RTKs can be activated through the binding of extracellular ligands.
Additionally, members of the Src family of tyrosine kinases have been shown to be associated with and be activated through cytokine binding to gp130 in cancer cells [ 26, 27].
This trans-membrane glycoprotein may be activated through the binding of related ligands, which leads to EGFR forming homodimers or heterodimers with its family members such as ErbB2/neu, ErbB3/HER3, and ErbB4/HER4.
Akt plays a critical role in endothelial cell migration and can be activated through the specific binding of VEGF165 to VEGFR-2, which then triggers the downstream VEGFR-2/PI3K/Akt signaling pathway.
To date, mounting evidence demonstrates that CAR can be activated through both classical ligand binding and ligand-independent mechanisms, with indirect activation appearing to be predominant.
In breast cancer, Met is thought to be activated through association with co-receptors or by binding to its ligand HGF produced by the tumor-associated stromal cells.
