ArticleCell cycle (Georgetown, Tex.)2010
Disparate chromatin landscapes and kinetics of inactivation impact differential regulation of p53 target genes.
Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Differential p53-Mediated Cellular Responses to DNA-Damaging Therapeutic Agents.International journal of molecular sciences · 2021Review
- Tumor suppressor p53: from engaging DNA to target gene regulation.Nucleic acids research · 2020Article
- ThePeerJ · 2020Article
- Ceramide Signaling and p53 Pathways.Advances in cancer research · 2018Review
- Mechanisms of transcriptional regulation by p53.Cell death and differentiation · 2018Review
- Putting p53 in Context.Cell · 2017Review
- Interactions of chromatin context, binding site sequence content, and sequence evolution in stress-induced p53 occupancy and transactivation.PLoS genetics · 2015Article
- Distinct phosphatases antagonize the p53 response in different phases of the cell cycle.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Dual effect of CTCF loss on neuroprogenitor differentiation and survival.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- A genetic screen identifies TCF3/E2A and TRIAP1 as pathway-specific regulators of the cellular response to p53 activation.Cell reports · 2013Article
- The histone acetyltransferase PCAF regulates p21 transcription through stress-induced acetylation of histone H3.Cell cycle (Georgetown, Tex.) · 2012Article
- The p53 circuit board.Biochimica et biophysica acta · 2012Review
- SUMO-activating SAE1 transcription is positively regulated by Myc.American journal of cancer research · 2012Article
- Stress-induced expression of p53 target genes is insensitive to SNW1/SKIP downregulation.Cellular & molecular biology letters · 2011Article
- Cooperative effects of Akt-1 and Raf-1 on the induction of cellular senescence in doxorubicin or tamoxifen treated breast cancer cells.Oncotarget · 2011Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The p53 transcription factor regulates the expression of genes involved in cellular responses to stress, including cell cycle arrest and apoptosis. The p53 transcriptional program is extremely malleable, with target gene expression varying in a stress- and cell type-specific fashion. The molecular mechanisms underlying differential p53 target gene expression remain elusive. Here we provide evidence for gene-specific mechanisms affecting expression of three important p53 target genes. First we show that transcription of the apoptotic gene PUMA is regulated through intragenic chromatin boundaries, as revealed by distinct histone modification territories that correlate with binding of the insulator factors CTCF, Cohesins and USF1/2. Interestingly, this mode of regulation produces an evolutionary conserved long non-coding RNA of unknown function. Second, we demonstrate that the kinetics of transcriptional competence of the cell cycle arrest gene p21 and the apoptotic gene FAS are markedly different in vivo, as predicted by recent biochemical dissection of their core promoter elements in vitro. After a pulse of p53 activity in cells, assembly of the transcriptional apparatus on p21 is rapidly reversed, while FAS transcriptional activation is more sustained. Collectively these data add to a growing list of p53-autonomous mechanisms that impact differential regulation of p53 target genes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.