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Second, we describe microarray analyses that can be used to compare gene expression differences between the allopolyploids and respective progenitors using appropriate experimental design and statistical analysis.
The importance of the underlying biology of breast tumors in predicting outcomes has been demonstrated by microarray analyses that identified molecular subtypes.
Alternative splicing can lead to altered isoform abundance that may not be apparent from microarray analyses that rely on probing of common exons, or RNA-seq analysis pipelines that only survey gene-level transcription.
It is particularly relevant to recent microarray analyses that suggest that co-expressed genes cluster along chromosomes or are spaced by multiples of a fixed number of genes along the chromosome.
This comparison is analogous to the microarray analyses that identified germline-enriched genes, in which animals with a germ line were compared to animals lacking a germ line [ 11, 12].
Notably, this result implies that the RNAs identified here as surveillance substrates would predominately be overlooked in microarray analyses that involve oligo dT) selection or priming for cDNA synthesis.
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One problem of microarray analyses is that expression data are often compressed to gene level annotation, which does not reflect alternatively spliced isoforms.
Microarray analyses suggested that RA down regulated genes that are biologically related to Erk regulatory pathways (Figure 1).
In addition to the biochemical data, microarray analyses revealed that METH preconditioning was associated with METH challenge-induced transcriptional responses that were substantially different from those observed in the absence of drug preconditioning.
The Sgk1 kinase is activated by IGF-1/phosphatidylinositol-3 kinase (PI3-K) signals, and data from several microarray analyses indicate that expression of Sgk1 is up regulated by mutations and treatments that inhibit the IGF-1/PI3-K pathway [ 53- 56].
Preliminary results from cDNA microarray analyses suggest that BRCA1 and BRCA2 have distinct gene expression profiles, which include genes that are involved in cell cycle control.
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