![]() ![]() ![]() Genes involved in type I diabetes mellitus were repressed by BEN but activated by TFII-I, suggesting that these transcription factors may act in a counterregulatory fashion in this pathway.įig. The pathway terms for ribosome, gap junction, apoptosis, and adherens junction were shown to be activated in both the BEN- and TFII-I-modulated gene list. The eight pathway terms were enriched in both BEN- and TFII-I-regulated genes, among which genes involved in neuroactive ligand–receptor interaction, calcium signaling pathway, and cytokine–cytokine receptor interaction were repressed. In the case of TFII-I regulated genes, the highest enrichment ( P < 1.2E-29) has been observed for the ribosomal pathway genes. The genes identified as being repressed by BEN were enriched with highest probability in the following pathways: neuroactive ligand–receptor interaction, complement and coagulation cascades, cytokine–cytokine receptor interaction, and hematopoietic cell lineage ( P < 3.7E-06), whereas those activated by BEN were predominantly enriched in cell cycle, proteasome, ribosomal pathway, and focal adhesion ( P < 1.6E-05). All genes present in microarray were taken as the background in calculation of the significance of enrichment ( P value) by using Fisher's exact test ( 14). BEN-modulated genes were shown to be significantly associated with 30 different KEGG pathway terms, and TFII-I-modulated genes were enriched in 10 pathways than would be expected by random chance. #Macvector download yale softwareFurther classification of BEN- and TFII-I-modulated genes by using bioinformatics software DAVID showed a significant ( P < 0.01) enrichment of genes involved in numerous pathways consistent with diverse biological functions of TFII-I proteins ( Fig. Our previous microarray studies identified 4,678 BEN- and 1,235 TFII-I-modulated genes ( 12, 13). ![]()
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