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Supporting this, we found cadherin1/E-cadherin/CDH1 to be dramatically up-regulated by pRb in our microarray assays, with an average fold-induction of 11.83 over pRb-null cells (P = 0.000, validated by qRT-PCR).
We showed that pRb-deficient cells have significantly reduced expression of OB-cadherin, which appeared among the transcripts that are up-regulated by pRb in our microarray assays, with an average fold-induction by pRb of 4.45 (P = 0.000).
Being in the red region of the spectrum, it offers the advantage of performing microarray assays with little or no background effects.
Activity tests, qRT-PCR experiments and microarray assays with xanthine dehydrogenase inducers demonstrated strong gene inducibility when cells were cultured on hypoxanthine and adenine and a lower level of induction with uric acid as the sole nitrogen source.
To determine whether AA had an impact on cell proliferation, we treated the same type of fibroblasts used in microarray assays with increasing concentrations of the drug and monitored the growth curves (Fig. 2a).
We performed microarray assays with RNA extracted from roots treated with 50 ppm FA after short (pooled from 1- and 3-h treatments) and long (24 h) exposure.
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Additionally, the reproducibility was defined as the proportion of identical calls made across the five microarrays assayed with identical DNA.
The signal intensities and the quality of the microarrays assayed with the samples collected in 2004 were higher than those of 2005, probably due to a better quality of the extracted RNA or to a higher metabolic activity in the 2004 samples (Additional file 1 Figure S2A).
Microarray assays performed with RNA amplified using our protocol demonstrate that the method results in low amplification bias and is highly reproducible.
Combining computational predictions with microarray assays, we identified 46 B. mori miRNAs, 13 of which were miRNA*s.
In conclusion, combining computational predictions with microarray assays, we identified 46 B. mori miRNAs, 13 of which were miRNA*s.
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