The B. napus expression datasets were downloaded from the BioProject (NCBI database: PRJNA358784). The data were obtained from various tissues at different B. napus developmental stages and under the induction of five different hormones (IAA, ABA, 6-BA, ACC, and GA3). The expression profiles of BnabHLHs were analyzed using the MeV v4.9 software ( -tm4/files/) [82] with the HCL method, and the heatmaps were drawn using the R package; The tissue high expression genes identified by z-score above3 in at least one of the organization samples [82]. All genes with FPKM
Recent studies have identified enhancer RNAs (eRNAs) as a class of regulatory ncRNAs that can increase the transcription of target genes [11]. There have been numerous reports that eRNAs are realised by interacting with RNA polymerase II and a co-transcription complex to mediate promoter-enhancer looping [12]. Enhancers may also regulate target gene expression via transcripts produced from the enhancer regions themselves [13]. It is well known that eRNAs can regulate the maintenance of hundreds of cells. Hence, eRNA dysregulation plays a key role in disease progression and tumour development [14]. In colon cancer, the lncRNA colon cancer-associated transcript 1 is transcribed from this super-enhancer belonging to eRNA, which regulates c-MYC oncogene expression [15]. Furthermore, most expression and function of genes involved in cancer signalling pathways are linked to eRNAs [16]. However, the numerous eRNAs involved in OC progression and prognosis have rarely been reported.
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Two clusters of pathways showed the most pronounced activation and deactivation. Five pathways were predicted to be activated across all doses, and all were involved in immune response or cell cycle regulation. There were 78 genes differentially expressed in these pathways, a majority of which were downregulated with respect to the control (Fig. 5B). A full list of genes can be found in Additional file 9: Table S7. In contrast to the pathway analysis of the mRNA targets, which showed the highest activation of several pathways after 4 Gy TBI, all activated pathways except natural killer cell signaling were consistently activated as the dose increased. We observed that radiation inhibits pathways relevant to xenobiotic metabolism and biosynthesis of lipids, including hormones. This is demonstrated by activation of LPS/IL-1 mediated inhibition of RXR function and inhibition of the super-pathway of melatonin degradation, among others. There were 79 genes involved in deactivation of these seven pathways, most of which were downregulated after TBI (Fig. 5C, Additional file 9: Table S7). 2ff7e9595c
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