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Thus, when studying microarray or proteomic data, we are dealing with fragmented traces of activity that are left behind by transient dynamic processes on different levels of cellular machinery.
Microarray or proteomic expression profiling is conventionally employed to identify disease-associated genes, however, traditional approaches for the analysis of profiling experiments may miss molecular aberrations which define biologically relevant subtypes.
For example, in microarray or proteomic experiments, researchers can map their experimental data through pathway mapping systems, such as ArrayXPath II [10], GenMAPP [11], MEGU [12], and Pathway Explorer [13], to gain a comprehensive understanding of cellular regulation and to explore the existence of alternative pathways after gene deletions or change in conditions.
Previous experiments suggest that genes sharing similar functions yield similar expression patterns in the microarray or proteomic experiments [ 1].
Therefore, over-expressing miR-519 in early-passage WI-38 cells followed by microarray or proteomic analysis will identify many transcripts directly regulated by miR-519.
Since seed pairing rules are neither sufficient nor necessary for miRNA-target functions [ 4, 14], they have usually been combined with microarray or proteomic analysis to find potential miRNA-target pairs[ 15- 17].
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Most of the ensemble models applied to drug sensitivity predictions have thus far used different base algorithms to extract features from one type of data (i.e., microarray 6 or proteomic 8.
While high-throughput data such as full genome sequences, microarray gene expression profiles, or proteomic data can be obtained quite efficiently for the pathogen in question, the context for proper interpretation of such data is often missing.
Simultaneous measuring of the expression of thousands of genes (gene microarray) or proteins (protein microarray) and detection of genomic or proteomic biomarkers, respectively, that are tightly linked to cancer development and/or progression have revolutionized the cancer research studies.
The reference database could also be integrated into a tool similar to the U.S. Food and Drug Administration's ArrayTrack to allow regulatory agencies to easily manage, analyze, and interpret omics data submitted by registrants or other government or academic laboratories using similar ecological species, testing protocols, and microarray, proteomic, or metabolomic platforms.
Although no major morphologic differences are recognized between CAFs and their normal counterparts, i.e. fibroblasts from the matched adjacent uninvolved mammary tissue or reduction mammoplasties, microarray and proteomic analysis revealed distinct mRNAs and protein expression profiles between them [ 6– 11].
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