To test the reversibility of this process, we treated the pre-assembled helical NLC preparations with sonication on ice and visualized the resulting particles by negative-stain EM.
To understand the molecular role of BMCC1 in this process, we treated NB cells with DNA-damaging reagents.
To investigate whether the observed differentiation mediated by Wnt was an irreversible process, we treated cells with Wnt3a and analysed their phenotype after its withdrawal.
To determine if the TGRL-induced drop in the number of Gr1low monocytes was a reversible process, we treated mice with P-407 for 2 weeks and then stopped the treatment.
To further characterize protease function during this process, we treated P. berghei-infected HepG2 cells 48 h post infection with 100 μm ml−1 leupeptin and antipain, two serine and cysteine protease inhibitors (Fig. 1A) and counted the detached cells 67 h after infection.
"Then, in another simple, low-temperature process, we treat the oils with hydrogen peroxide and formic acid, and then add acrylic acid to get the characteristics we want.
To examine cellular processes regulating phenotypic changes, we treated MCF-7 cells with selective inhibitors affecting two major signalling pathways induced by ErbB receptors in this cell line, i.e. the ERK/MAPK and PI3K pathways.
In order to determine the effect of PAQG on the level of p-AMPK in the differentiation process of 3T3-L1, we treated the cells with 20 μM PAQG or vehicle, and collected cell samples at different time of the process.
To determine whether bexarotene prevents cancer at the early stages during the multistage process of mammary carcinogenesis, we treated MMTV-erbB2 mice with bexarotene for 2 or 4 months.
Finally, to test the involvement of proteasome-dependent degradation in the process of CDCP1 down-regulation, we treated PC3 cells with the proteasome inhibitor, MG132, and found that inhibiting the proteasome prevented the KAI1-dependent reduction in CDCP1 levels.
Despite our implicit understanding that non-equilibrium mechanisms play pivotal roles in many biological processes, we often explicitly treat eukaryotic gene regulation as if it were an equilibrium process.
