Non-canonical and canonical pathways can inhibit each other, and even non-productive interactions (for example Wnt5A Lrp6) can compete with normal signaling activities (for example, activation of the non-canonical target Rac1) [53], [54].
For example, activation of the mitogen-activated kinase (MAPK) pathways by other growth factors can lead to inhibitory phosphorylation of SMAD2 and SMAD3 in the regulatory "linker region" and thus inhibition of signaling propagation [ 36].
For example, activation of CIPK20 is required to activate the ABA signaling pathway involved in seed germination and growth elongation inhibition in A. thaliana (Gong et al. 2002).
For example, activation of Gα12/13, Gαq/11, or Gαi/o induces YAP/TAZ activity, whereas activation of Gαs represses YAP/TAZ activity [ 27].
For example, activation of EphA by its ligand leads to a transient inhibition of Rac1 activity, concomitant with RhoA activation [30], [31].
In addition, APA can be dynamically regulated in response to extracellular signals, for example activation of neuronal cells [29].
For example, activation of expression from genes in clusters #11 and #9 rapidly follows the activation of FGF8 expression.
For example, activation of Xtwn requires Smad3 binding to the Smad binding elements (SBEs); c-myc activation needs Smad4 binding to the Lef/Tcf binding elements 1 (TBE1).
For example, activation of integrin αIIbβ3 leads to a stable adhesion of circulating platelets and further changes in the cell shape.
For example, activation of phosphorylation pathways by protein kinase A was able to restore voltage-dependent potentiation of L-type Ca2+ channels in mdx fibres [67].
For example, activation of the A2BR on pulmonary fibroblasts promotes their differentiation into myofibroblasts and hence increases the deposition of collagen and fibrosis [20].
