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Second, using plants transformed with two readily measurable genetic markers, we measured the competitive ability of transformed pollen with native pollen in natural populations and, in glasshouse arenas, the ability of adult Manduca sexta moths to transfer pollen between plants.
In order to confirm the p53-dependent arrest footprint defined by these markers, we measured the p53-dependent transactivation of 4 among the selected genes by qRT-PCR in HCT 116 p53+/+ cells treated with different DNA-damaging agents.
As non-skeletal markers, we measured serum levels of high-sensitivity CRP and homocysteine.
As additional markers, we measured urinary excretion of NO (UNOx) and l-arginine to asymmetrical dimethyl-arginine to asymmetricalplasma.
Using these markers, we measured the levels of genetic variation among and within all populations sampled and inferred the phylogenetic tree for these species.
To more directly examine the effects of ATO on stem cell markers, we measured levels of SOX2 and CD133 mRNA after 24 hours of treatment.
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For each marker, we measured its additive and dominant effect using flowering data gathered along pedigrees.
As epithelial marker we measured E-cadherin and as mesenchymal markers N-cadherin and vimentin by Western blot.
Using pCHK1S345 as a marker, we measured ATR inhibition by NU6027 in GM847KD and human breast cancer, MCF7 cells.
For each marker, we measured at least two variables: the intensity of the signal (integrated absorbance) and the percentage of positive stained area/nuclei, based on the binary images.
In diploid cells expressing the Vph1-GFP marker
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