Those authors proposed a model in which induction of VEGF by ionizing radiation contributes to the protection of tumour vessels from radiation-mediated cytotoxicity.
Viral infections, on the other hand, appear to thrive on host Nrf2 activation, as illustrated by a number of examples in which induction of Nrf2 activity favours virus proliferation.
These findings support a model in which induction of apoptosis by AITC stems primarily from activation of ROCK1 and PTEN, and inactivation of PI3K, leading in turn to activation of PP1 and PP2A, resulting in dephosphorylation of cofilin, which binds to G-actin and translocates to mitochondria, culminating in the dysfunction of mitochondria, release of cytochrome c and apoptosis.
To elucidate potential mechanisms by which the induction of arthritis is suppressed in Nampt+/− mice, we measured the serum levels of the arthritogenic anti-mouse CII auto-antibody, which plays a crucial role in the initiation of CIA7.
The inducibility of Hsp27 and αB-crystallin transcription by various stresses is exerted by HSF-dependent mechanisms, by which concomitant induction of Hsp27 and αB-crystallin expression is observed.
Although the mechanisms by which the induction of the heat shock response might improve organ perfusion and attenuate organ damage are not fully understood, it has been demonstrated that the heat shock response inhibits cytokine-mediated expression of inducible nitric oxide synthase [ 25].
Cell cultures were grown at 37 °C with a rotary shaker until an A600 of ∼0.6 was reached, after which induction was initiated by the addition of 1.0 mM isopropyl thiogalactoside (IPTG).
We hypothesised that the main mechanism by which labour induction reduces the risk of a high-risk situation may be through its effect on the time from admission to delivery.
The mechanisms by which Cas inhibits induction of autophagy and affects cell death pathways are currently being investigated.
The exact mechanism by which hyperthermia, via induction of the heat shock response, appears to modulate the immune response to sepsis is thought to be through inhibition of IKK proteins [ 45].
