Sentence examples for vitro we find from inspiring English sources

Using a methyltransferase footprinting assay on isolated nuclei (in vitro), we find that the chromatin at these fragile zones is accessible.

In contrast to the effect of antibiotics in vitro, we find that the fraction of actively dividing bacteria remains relatively high throughout the course of a chronic infection in vivo and increases in response to antibiotics.

By measuring the paclitaxel-microtubule association constant and performing microtubule-associated experiments in cells and in vitro, we find that EB1 increases the binding affinity between paclitaxel and microtubules and promotes paclitaxel-mediated tubulin polymerization and stabilization.

Using photoconductive stimulation to trigger high frequency action potentials in rat hippocampal neurons in vitro, we find that activity functions as an attractive cue for growth cones in the local environment.

When we now follow cavity formation in embryos developing either in vivo or in vitro, we find a requirement not for apoptosis but, instead, for polarization of EPI cells into a rosette-like structure.

Although DWA1, 2, and 3 all interact with both DDB1A and DDB1B in vitro, we find that germination in ddb1a is more sensitive to 100 mM NaCl and 200 mM Mannitol than germination in ddb1b-2 or wild type.

Despite finding several candidates that work in vitro, we found that only one peptide can competently activate the expression of FLO11 in haploid yeast cells.

Similar to our findings using miR-146 inhibitors in vitro, we found that levels of HuR mRNA and protein were increased in the hearts of miR-146a−/− mice (Fig 8C), suggesting that HuR is also a target of miR-146a in vivo.

In vitro, we found that neochlorogenic, chlorogenic, and caffeic acids induce the proliferation and repress the alkaline phosphatase activity of primary preosteoblasts in a dose-dependent manner.

By testing lipidoids and DOTAP for innate immune-receptor-activating properties in vitro, we found that neither lipidoids nor DOTAP activate human Toll-like receptor (TLR) 2, 3, 7, and 9.

However, using a molecular beacon assay to test lesion removal in vitro, we found that XRCC1 facilitates AAG-initiated excision of two key NO-induced DNA lesions: 1,N6-ethenoadenine and hypoxanthine.