ArticleNucleic acids research2006
En masse nascent transcription analysis to elucidate regulatory transcription factors.
Article in Nucleic acids research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed.
- Array-based nuclear run-on analysis.Methods in molecular biology (Clifton, N.J.) · 2012Article
- Cloning and characterization of the NPCEDRG gene promoter.Molecular and cellular biochemistry · 2011Article
- Time-dependent c-Myc transactomes mapped by Array-based nuclear run-on reveal transcriptional modules in human B cells.PloS one · 2010Article
- TREX1 acts in degrading damaged DNA from drug-treated tumor cells.DNA repair · 2009Article
- Hypoxic transcription gene profiles under the modulation of nitric oxide in nuclear run on-microarray and proteomics.BMC genomics · 2009Article
- A general mechanism for transcription regulation by Oct1 and Oct4 in response to genotoxic and oxidative stress.Genes & development · 2009Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Despite exhaustively informing about steady-state mRNA abundance, DNA microarrays have been used with limited success to identify regulatory transcription factors (TFs). The main limitation of this approach is that altered mRNA stability also strongly governs the patterns of expressed genes. Here, we used nuclear run-on assays and microarrays to systematically interrogate changes in nascent transcription in cells treated with the topoisomerase inhibitor camptothecin (CPT). Analysis of the promoters of coordinately transcribed genes after CPT treatment suggested the involvement of TFs c-Myb and Rfx1. The predicted CPT-dependent associations were subsequently confirmed by chromatin immunoprecipitation assays. Importantly, after RNAi-mediated knockdown of each TF, the CPT-elicited induction of c-Myb- and/or Rfx1-regulated mRNAs was diminished and the overall cellular response was impaired. The strategies described here permit the successful identification of the TFs responsible for implementing adaptive gene expression programs in response to cellular stimulation.
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Registered trials
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