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PTI often activates downstream mitogen-activated protein kinase (MPK) cascades and defense response genes.
The activation of STPs often activates downstream transcription factors (TFs), which then bind to their target genes to turn on or off various transcription programs.
The delivered vector often activates the innate immune response that leads to activation of antigen-presenting cells (APCs) against the vector and the therapeutic gene.
Transcription often activates neighbouring genes, for instance, genes that respond early to external stimuli.
This kind of cellular stress often activates other metabolic pathways as well, such as fatty acid synthetase (FAS) pathways [ 59].
Oncogenic signalling often activates the Erk pathway, which is a known mediator of cell proliferation, cell survival, angiogenesis and cell migration (reviewed in [ 36]).
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Yet Ras genes and Braf, while often activated in cancer cells, are infrequent targets for activation in neuroblastoma.
Chk1 and Chk2 are often activated by ATM and ATR, resulting in a cascade of activation of further downstream signals.
The TORC1 pathway is often activated in human cancers and rapamycin exhibits anti-tumorigenic activity (Guertin & Sabatini, 2007).
IP3Rs located at the surface of the ER are often activated via the production of phospholipase C PLCC) following the activation of group I mGluRs.
ERK1/2 is often activated by growth factors [12], while p38 and SAPK/JNK are stress-activated protein kinases, which respond to cellular stress and inflammatory cytokines [14, 15, 17].
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