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The enriched KEGG pathways [ 32], microRNA (miRNA) target gene sets [ 33, 34] and GO terms [ 35] identified by gene set analysis also support ClustEx predictions.
Examination of the existing literature reveals that, in addition to DMBA-induced mammary tumors, other mouse models that show a similarly high presentation of squamous-like mammary tumors are the Brg1 +/− [ 17] and Pik3ca-H1047R [ 18] models, the squamous tumors of which were shown by gene set analysis to be similar to claudin-low human breast tumors [ 19].
Comparing the subpopulations of different growth rates with RP, biologically significant differences were detectable as tested by gene set analysis (GAGE (Luo et al. [2009]) and Globaltest (Goeman et al. [2006])) (Figure 4b and 4c).
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These single-gene results were paralleled by a gene set analysis on 1,230 annotated genes ranked by dN/dS, where functional categories involved with heat shock proteins, signal transduction and in the regulation of transcription and nucleic acids were more likely to contain genes with high dN/dS (Additional File 3).
Gene-Ontology analysis was performed separately on the set of genes with significantly higher expression in the neo aortic samples and those with significantly higher expression in the w6 samples by model-based gene set analysis [25] using the Ontologizer [65].
We were able to confirm these data by using positional gene set analysis, demonstrating that cytoband 1p31 contains a cluster of genes that are overexpressed in ADLD.
Significant genes including ACTN1, CCND1, HCLS1, ITGB5, PFN2, PTPRC, RAB13, and WAS, which are adhesion-related molecules that were identified by both SAM and gene set analysis, and showed interaction in the genetic network with the integrin signaling pathway.
Many of these correspond to signals that hover below GWS in GWAS studies, and when analyzed together for commonalities of pathways or other processes by means such as gene set analysis, as a group are significantly associated with these phenotypes.
We report sound results of gene sets associations that remained undetected by the conventional one-dimensional gene set analysis in several examples.
We then conducted gene set analysis by GSA on the two factors.
Using this mixed model gene set analysis and by combining weak signals of differential expression across genes within the same gene set, we identified gene sets that were differentially expressed between MS and healthy controls in unstimulated PBMC.
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