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Several recent studies investigated activation of glycolysis during brain hypoxia exposure.
We investigated activation of checkpoint signaling and induction of cell cycle arrest following exposure of iPS cells to γ-radiation.
We next investigated activation of the Akt signaling pathway in response to G-CSF, which we have previously shown to be important in G-CSF-mediated cell survival and proliferation.
To find an explanation for this dissociation of phenotypes, we investigated activation of IGF signaling under acute oxidative stress.
We investigated activation of PERK and eIF2α in postmortem brains from subjects with PSP and AD, as well as from normal elderly subjects.
In the model, an inhibiting effect of RsbR is indistinguishable from an activation of RsbR-P, therefore we investigated activation of RsbT by RsbR-P instead.
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Participants completed a rapid serial visual presentation paradigm designed to investigate activation of attentional networks to behaviorally-relevant targets and contingent attention capture by task-irrelevant distractors.
To further investigate activation of the complement system by the different influenza virus infections, immunoblot analyses of BAL were performed.
To corroborate the findings that cocaine and gp120-mediated toxinvolvedvolved the apoptotic pathway, we next sought to investigate activation of caspase-3.
Preparation of metal-free enzymes is required for investigating activation of many metalloenzymes.
To investigate activation of c-MET in the drug-resistant cells, we confirmed the levels of p-MET protein.
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