TFII-I Target Genes

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It is important to understand the downstream events that occur when there is a loss of genes like GTF2IRD1, GTF2IRD2 and GTF2I such as in the case of WBS. These genes encode members of the TFII-I transcription factor family that are involved in diverse pathways essential for proper embryonic development and cellular processes such as axon guidance, calcium signaling, cell cycle and immune response (Chimge et al., 2008.) To find TFII-I target genes the researchers have conducted a genome wide search in human and mouse genome and have used ChIP (chromatin immunoprecipitation) and RNAi to identify new TFII-I target genes (Chimge et al., 2007; Chimge et al., 2007.) They have analyzed in mouse embryonic fibroblasts (MEFs) promoter regions of the…show more content…
Those repressed by BEN are those involved in pathways such as neuroactive ligand-receptor interaction, complement and coagulation cascades, cytokine-cytokine receptor interaction and hematopoietic cell lineage. While those activated by BEN are involved in cell cycle, proteasome, ribosomal pathway and focal adhesion. Whereas GTF2I protein product TFII-I modulates genes involved in 10 pathways and significantly involved in the enrichment of the ribosomal pathway genes (Chimge et al., 2008.) It was also found that genes involved in type I diabetes mellitus were modulated by both BEN and TFII-I however with opposite roles; BEN repressed whereas TFII-I activated. It was also found with microarray analysis that while BEN and TFII-I modulate over 96 of the same genes, BEN modulates around 601 genes whereas TFII-I modulates around 11 genes of the 1725 genes of the consensus…show more content…
It was found that both were recruited for the proximal promoters of Bax, Shrm, Cfl-1, Ezh2, Epc1, and Ccnd3. Promoters sites that only recruited BEN included Tgfb2, Nedd8 and Opn whereas those of TFII-I was only Hdac1. No binding was detected for Lhx1, Tgif, Fgf11, Ldb1, Cdk5rap1, and Hdac7a, which lead the researcher to believe that the most likely explanation was that they are not the primary target genes and most likely their modulation, occurs via secondary mechanisms (Chimge et al.,

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