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The binding of a transcriptional activator to the promoter region of a gene suggests that the activator has a regulatory effect on the gene, but it is also possible that the activator does not fully or even partially control the gene.For this reason, we have identified the set of genes GENES DEVELOPMENT where factor binding correlates with gene expression, an approach that produced highly accurate information on transcription factor function in previous studies with other factors. We have also confirmed the importance of EF binding to several of the novel targets identified here by examining gene expression in cells that lack the p and p repressors recruited by EF.We found that expression of each of these targets was significantly deregulated in cells lacking p and p.These findings confirm the functional relevance of EF binding in vivo to targets identified in our location analysis.A substantial number of these EF target genes have not been previously linked to EF function.Several important conclusions can be drawn from this work   based on the functional clustering of the EF targets we have identified.DNA <a href="https://www.ncbi.nlm.nih.gov/pubmed/246659320">buy Ferrous fumarate</a> replication A role for EF in the activation of several DNA replication genes has been well established.Known EF targets include genes encoding proteins involved in the initiation of replication, and the enzymatic synthesis of DNA. Our studies have expanded this list to include additional nucleotide synthesis and replication factor genes.However, an emerging idea from recent studies suggests that EF may be required to regulate cyclin gene expression beyond S phase, and expressionprofiling identified several potential downstream targets involved in mitosis. However, given the caveats associated with this type of experiment described above, it was not possible to distinguish direct from indirect targets.We identified a significant number of genes that function in mitosis.Our experiments strongly suggest that EF plays a direct role in regulating several genes involved in mitosis.These genes are involved in the full spectrum of repair processes, including mismatch repair, homologous recombination. Many of the genes isolated in this screen are members of multimeric complexes, and our data suggest that they may be coordinately regulated.Many of these genes appear to be bound by EF in quiescent cells when each is inactive and by the EF activator in GS phase cells when each is expressed. Therefore, our findings link the processes of DNA replication and repair in mammalian cells and suggest that their expression could be regulated through a common factor, EF.The identification of p as an EF target was unanticipated, because the p promoter lacks a recognizable EF consensus site. This finding may be explained by the indirect recruitment of EF by additional promoterbound factors.Our results suggest that EF may also directly control p expression levels.This finding is also intriguing in light of previous reports implicating an essential role for both p and the pRB family in the G DNA damage arrest checkpoint. These proteins have been shown to interact, again suggesting that this checkpoint may be controlled coordinately by EF.However, as cells reenter the cell cycle and approach S phase, it is necessary to activate genes needed for repair of the DNA damage that occurs during replication.

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