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Meanwhile, microbial products such as LPS were demonstrated to trigger a program of DCs maturation which enables DCs to activate T cells [ 14].
Indeed, simple compressive stress resulting from bronchoconstriction has been demonstrated to trigger a pro-fibrotic response reminiscent of remodelling in the absence of eosinophilic inflammation (4).
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Previous studies have linked induction of EMT under hypoxic conditions to Notch signalling [ 33], whilst ectopic expression of Notch1 intracellular domain (N1CD) has been demonstrated to trigger an EMT in epithelial cancer cells [ 34].
Oxidized lipids have been demonstrated to trigger autophagy in endothelial cells as a protective mechanism to prevent early processes of atherosclerosis.
Mechanical muscle injury by daily repeated micromultipunctures for 14 days has been demonstrated to trigger fibrotic lesions in mdx hindlimb muscles that consequently display a similar pattern to diaphragm muscles [ 85].
Hypomethylation contributes to carcinogenesis in a variety of ways and, in mice, has been demonstrated to trigger the initiation of cancer [ 19].
Dr. Fisher believes it is triggered by higher levels of vasopressin and oxytocin, which have been demonstrated to trigger attachment in animals.
Among the proposed mechanisms accounting for the proapoptotic effect of anion channels, cellular acidification due to anion influx has been demonstrated to trigger mitochondria apoptotic cascade involving Bcl-2.
The glycosylphosphatidylinositol (GPI) of T. gondii was demonstrated to trigger TLR4 signaling pathways [ 8– 10].
In tobacco, PVD358, PVD374 and PVD417 have all been demonstrated to trigger ISR [ 132].
The oligomerization of amyloid peptides and AMPs have been demonstrated to trigger membrane leakage.
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