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Thus, the authors have made an important, if tentative, contribution towards bridging the gap between emerging microarray experimental technologies and the bioinformatics tools needed to interpret their output.
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Due to the advances in high-throughput experimental technologies, an increasing number of large-scale microarray studies have been conducted to identify ageing associated genes in human and model organisms [ 2- 7].
The recent advancement of experimental technologies such as chromatin immunoprecipitation followed by massively parallel DNA sequencing (ChIP-seq) [ 26] or microarray hybridization (ChIP-chip) [ 27] enables us to more accurately determine genome wide occupation of TFs.
The classes one-color microarray experimental process and two-color microarray experimental process also specialize DNA microarray experimental process.
The two experimental technologies available for large-scale gene expression analysis are: 1) DNA sequencing-based serial analysis of gene expression (SAGE) and expressed sequence tag (EST) approaches and 2) dot-blot based microarray analysis.
In the 1990s, DNA microarray or DNA chip as a novel biological experimental technology was developed, which enables the comprehensive measurement of the expression levels of hundreds of genes, simultaneously.
A powerful high-throughput experimental technology, called the transcription factor knockout microarray (TFKM) [ 8], is widely used to investigate the regulatory relationships between TFs and genes.
To date, Chromatin Immunoprecipitation coupled with microarray chip (ChIP-Chip) or deep sequencing (ChIP-Seq) is the predominant experimental technology for obtaining genome-wide maps of histone modifications.
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In this study, based on microarray technology and experimental approaches, we suggest that NLC1-C functions as a repressor to regulate the expression of miR-320a and miR-383 by binding to Nucleolin in the nucleus and in the cytoplasm, NLC1-C is the direct target of miR-320a and miR-383 in human spermatogenesis.
Some microarray technologies and experimental designs produce intensity values whose absolute values cannot always be compared directly from gene to gene.
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