Sentence examples for mechanisms we treated from inspiring English sources

To define the mechanisms, we treated primary mouse microglia from wild type mice with various concentrations of morphine for different time periods and examined the expression of TLR9 by quantitative real time RT-PCR and Western blot analysis.

To further investigate such mechanisms, we treated hepatocellular carcinoma cell lines, Huh7, HepG2 and PLC cells with BBP (1 μM).

To obtain better insights into toxicity mechanisms, we treated juvenile Atlantic cod (Gadus morhua) with PCB 153 (0.5, 2 and 8 mg/kg body weight) for 2 weeks and performed gene expression analysis in the liver using oligonucleotide arrays.

To explore the underlying molecular mechanisms, we treated bladder cancer cells with HA-1077 and then examined changes of the GTP-bound active form of RhoA and expression of its downstream effector ROCK.

To test these two possible mechanisms, we treated embryos with either jasplakinolide (Jas), which disrupts actin turnover by stabilizing actin filaments (Bubb et al., 1994; Cramer, 1999), or with Y27632, a Rho kinase inhibitor that indirectly inhibits myosin-2 (Davies et al., 2000).

In order to provide additional support for this hypothetical mechanism, we treated wt and BCL11B-overexpressing cells with the HDAC inhibitor trichostatin A (TSA).

To address this potential mechanism, we treated the Fus1 KO mice with an inhibitor of pathogenic oxidative reactions, pyridoxamine (PM).

To study this mechanism, we treated lysate of ALDH1L1-expressing cells, accumulating high levels of Bid, with recombinant caspase-8.

In order to analyze AMPK involvement in this mechanism, we treated cells with compound C and observed a reversion of both metformin and VEGF-mediated ERK1/2 phosphorylation effects.

To achieve long term inhibition of Gli1 by another mechanism, we treated 231 cells continuously for 8 days with the small molecular inhibitor of Gli-mediated transcription, HPI-1.

To minimize the possibility that an off-target effect of 3-IB-PP1 blocks Erk phosphorylation by a CskAS-independent mechanism, we treated WT BMDMs with a combination of zymosandep and increasing concentrations of 3-IB-PP1 and found no suppression of Erk phosphorylation.