We based this analysis on a set of previously-identified housekeeping genes and identified 41 genes through ANOVA and K-means clustering analysis.
We discovered pancancer hyper and hypomethylated genes and identified novel methylation driven subgroups with clinical implications.
We characterized olfactory receptor (OR) genes and identified 32 and 33 OR-like genes in the BP and PM genomes, respectively (Supplementary Table 16).
Kobayashi et al.50 demonstrated that Nrf2 suppresses inflammation through redox control, by opposing the transcriptional upregulation of proinflammatory cytokine genes and identified Nrf2 as the upstream regulator of cytokine production.
We evaluated the AS of genes and identified differentially alternatively spliced (DAS) genes for which the transcriptional level of isoforms of these genes differed considerably between the different cell types.
We have examined the expression of several known genes and identified novel ones in the adult rat hippocampus after a mild, transient, hypovolemic and hypotensive, global ischemic stress.
Bridging these data and data from mRNA profiling provided functional explanations for many of these genes and identified previously unknown relations between alpha-synuclein toxicity and basic cellular pathways.
Using gene coexpression network analysis, we derived functional modules, regulatory mediators, and higher-order topological relationships between genes and identified 50 gene coexpression modules in developing myocardium that were not present in normal adult tissue.
Overlaying HT-ChIP data on gene-expression dynamics shows that many TF-DNA interactions are established prior to the stimuli, predominantly at immediate-early genes, and identified specific TF ensembles that coordinately regulate gene-induction.
We sequenced two positional candidate genes and identified a homozygous frameshift mutation in the gene encoding the 135 kDa centrosomal protein (CEP135), located in the linkage interval on chromosome 4, in both affected children.
To finely map the basis of heterogeneous responses during infection, we clustered cells by differential expressed genes and identified host pathogen co-stages of infection in groups of infected macrophages and phagocytosed C. albicans pairs that showed similar gene expression profiles (Figs. 3a and 4a).
