Evidence map›Paper›PMID 22894900›Full record

ArticleCell cycle (Georgetown, Tex.)2012

Mutant p53 is a transcriptional co-factor that binds to G-rich regulatory regions of active genes and generates transcriptional plasticity.

Timo Quante, Benjamin Otto, Marie Brázdová, Iva Kejnovská, Wolfgang Deppert, Genrich V Tolstonog

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 63 citations in OpenAlex.

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  15. The Rich World of p53 DNA Binding Targets: The Role of DNA Structure.International journal of molecular sciences · 2019
    Review
  16. P53-R273H mutation enhances colorectal cancer stemness through regulating specific lncRNAs.Journal of experimental & clinical cancer research : CR · 2019
    Article
  17. Article
  18. Article
  19. p53 Is Active in Human Amniotic Fluid Stem Cells.Stem cells and development · 2018
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 4 countries.

Timo QuanteHeinrich-Pette Institute, Hamburg, Germany.
Benjamin Otto
Marie Brázdová
Iva Kejnovská
Wolfgang Deppert
Genrich V Tolstonog
Leibniz Association · DECzech Academy of Sciences, Institute of Biophysics · CZMasaryk University · CZUniversität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The molecular mechanisms underlying mutant p53 (mutp53) "gain-of-function" (GOF) are still insufficiently understood, but there is evidence that mutp53 is a transcriptional regulator that is recruited by specialized transcription factors. Here we analyzed the binding sites of mutp53 and the epigenetic status of mutp53-regulated genes that had been identified by global expression profiling upon depletion of endogenous mutp53 (R273H) expression in U251 glioblastoma cells. We found that mutp53 preferentially and autonomously binds to G/C-rich DNA around transcription start sites (TSS) of many genes characterized by active chromatin marks (H3K4me3) and frequently associated with transcription-competent RNA polymerase II. Mutp53-bound regions overlap predominantly with CpG islands and are enriched in G4-motifs that are prone to form G-quadruplex structures. In line, mutp53 binds and stabilizes a well-characterized G-quadruplex structure in vitro. Hence, we assume that binding of mutp53 to G/C-rich DNA regions associated with a large set of cancer-relevant genes is an initial step in their regulation by mutp53. Using GAS1 and HTR2A as model genes, we show that mutp53 affects several parameters of active transcription. Finally, we discuss a dual mode model of mutp53 GOF, which includes both stochastic and deterministic components.

Indexed as

Binding SitesCell Cycle ProteinsCell Line, TumorChromatin ImmunoprecipitationGene Expression ProfilingGene Expression Regulation, NeoplasticGPI-Linked ProteinsGuanosineHumansMutationPolymerase Chain ReactionReceptor, Serotonin, 5-HT2ARegulatory Elements, TranscriptionalTranscription, GeneticTumor Suppressor Protein p53Cell Cycle ProteinsGAS1 protein, humanGPI-Linked ProteinsGuanosineReceptor, Serotonin, 5-HT2ATumor Suppressor Protein p53

Identifiers

PMID22894900
PMCPMC3466528
OpenAlexW2070062778

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.