Binding of FGF and especially VEGF, which is considered a major molecule controlling blood vessel morphogenesis, to their tyrosine kinase receptors activates multiple downstream molecules involved in different signalling pathways that lead to increased vascular permeability, cell migration and proliferation [3].
A single activated receptor may then activate multiple downstream molecules, resulting in the signal amplification of a zymogen cascade.
Upon binding to its receptor RANK on the cell surface of osteoclast precursors, RANKL induces the recruitment of adaptor molecules such as tumor necrosis factor receptor-associated factor 6, which activates multiple downstream signaling molecules including mitogen-activated protein kinases (MAPKs) and NF-κB.
Predictably, DsbA disruption affects multiple downstream effector molecules, resulting in pleiotropic effects on the virulence of important human pathogens.
Interestingly, we observed that the signal intensities for phospho-IGF-1R and total IGF-1R were also decreased on the protein array, which raised the possibility that PTK6 modulates activation and/or expression of the receptor itself, thereby influencing multiple downstream signaling molecules.
IL-21 binding with this receptor leads to the activation of multiple downstream signaling molecules, including JAK1, JAK3, STAT1 and STAT3, therefore affects the innate and adaptive immune responses by inducing the differentiation, proliferation and activity of multiple target cells.
Pyk2-mediated functions were performed by activating multiple downstream signaling molecules, including ERK, p38, c-Src and paxillin, which led to the differential regulation of cell invasion in various cell types [ 31- 34].
For selected miRNAs, namely miR-149, miR-148b, miR-326, and miR-520a-3p miR-520a-3p miR-520a-3pultaneous doweregulation of the ErbB3 receptor andemonstratedownstheam simultaneouslecules, explaining their efficient downregulationRG respofses and ascribing thethErbB3ireceptorentiandcontext-dependent tumultipleressive functions.
Intracellular signaling networks comprising multiple RTKs and their downstream molecules may confer the molecular complexity and compensatory pathway against TKIs-mediated inhibition of tumor cell growth.
That is, the output of an upstream process is a molecule (or often more formally the production rate of this molecule) that is consumed as input by multiple downstream processes.
Its biological processes involve inflammation, angiogenesis, and cell survival and are mediated through the fibroblast growth factor-inducible molecule 14 (FN14) receptor, a finely tuned, inducible receptor encompassing multiple downstream signalling cascades.
