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Consistent with these findings, Cai et al. demonstrated that glucose deprivation induces ROS production to activate AMPK in pancreatic β cells [45].
Flagellins are recognized by TLR5 as pathogen-associated molecular patterns (PAMPs) and induce cytokine production to activate the host innate immune system.
These findings suggest for the first time that RRM2 can induce ROS production to activate the ERK1/2 pathway, which then promotes VEGF expression in cervical cancer cells.
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Perhaps of greater importance is the established ability of GLP-1 to stimulate cAMP production and to activate both PKA and Epac [19], [20].
Thus, while emotional prosody perception and also prosody production are known to activate the right hemisphere each [2], "mirror" regions for prosody seem to be stronger in the left hemisphere.
DCA-induced superoxide anion production is expected to activate the SOD/CAT oxidative stress pathway.
Dermal IGF-1 production is necessary to activate the IGF-1 receptor present on basal keratinocytes in order to preserve this appropriate UVB response.
We further suggest that in hypoxia, production of H2O2 to activate signalling pathways may be also mediated by decreased oxidized cytochrome c and less superoxide scavenging.
In aging vessels, increased production of ROS fails to activate Nrf2, resulting in increased blood vessel sensitivity to the deleterious effects of ROS [ 48].
We demonstrate here that, as a result of SE-triggered NO production, extracellular adenosine fails to activate the cAMP-mediated anti-oxidative pathway.
The second key assumption of FBAwMC, namely that cells have evolved regulation mechanisms to activate production of enzymatic machinery for the pathway giving optimal growth rate [ 22], relates closely to the explanation proposed by Molenaar et al. [ 12].
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