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Microarrays offer a compact solution for massively parallel screening.
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Therefore, orders-of-magnitude more powerful computing resources would be necessary for massively parallel screens.
Improvements in sequencing technologies have evolved into new paradigms for analyzing tumor specimens; massively parallel screens can examine patient samples for potentially actionable targets.
A recent study by Arnold et al. (2014) used massively parallel enhancer screens (Arnold et al. 2013) to find that hundreds of novel CRMs have emerged on the scale of approximately 10 Myr, lending credibility to our theoretical findings.
Using massively parallel sequencing we screened the OCT1 gene for amino acid substitutions and characterized them for their effects on subcellular localization and transport activity using 10 known OCT1 substrates.
Targeted massively parallel sequencing permits screening of genomic regions for multiple samples simultaneously, and thus is a powerful and cost-effective tool for characterizing mutations in contexts where multiple genes or pathways are involved[ 1, 13- 15].
To address these limitations, we previously developed Hi-Plex, a polymerase chain reaction (PCR) massively parallel sequencing strategy for screening panels of genomic target regions.
We applied massively parallel sequencing to screen for coding polymorphisms in 1,079 unrelated individuals from 53 populations worldwide.
The design of these substrates arose from a massively parallel high-throughput microarray screening process using peptide nucleic acid (PNA) encoding technology, allowing the identification of detailed substrate specificities of any protease.
For example, nonbiased massively parallel sequencing-based carrier-screening assays show that every individual carries an average of 2.8 mutations among genes known to cause severe pediatric disease in the recessive form.
Here, we performed massively parallel sequencing and exonic CNV screening of 12 isoprenoid genes in 134 index PK patients (61 familial and 73 sporadic) and identified causal mutations in three novel genes (PMVK, MVD, and FDPS) in addition to MVK in the mevalonate pathway.
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