ReviewOncogene2007
Changing the p53 master regulatory network: ELEMENTary, my dear Mr Watson.
Review in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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.
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.
Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Altered-function p53 missense mutations identified in breast cancers can have subtle effects on transactivation.Molecular cancer research : MCR · 2010Trial
- Tumor suppressor p53: from engaging DNA to target gene regulation.Nucleic acids research · 2020Article
- Revealing a human p53 universe.Nucleic acids research · 2018Article
- The novel p53 target TNFAIP8 variant 2 is increased in cancer and offsets p53-dependent tumor suppression.Cell death and differentiation · 2017Article
- Bridged Analogues for p53-Dependent Cancer Therapy Obtained by S-Alkylation.International journal of peptide research and therapeutics · 2016Article
- Adaptive methylation regulation of p53 pathway in sympatric speciation of blind mole rats, Spalax.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Article
- Human single-nucleotide polymorphisms alter p53 sequence-specific binding at gene regulatory elements.Nucleic acids research · 2011Article
- Article
- Nitric oxides mediates a shift from early necrosis to late apoptosis in cytokine-treated β-cells that is associated with irreversible DNA damage.American journal of physiology. Endocrinology and metabolism · 2009Article
- The expanding universe of p53 targets.Nature reviews. Cancer · 2009Review
- A regulatory loop composed of RAP80-HDM2-p53 provides RAP80-enhanced p53 degradation by HDM2 in response to DNA damage.The Journal of biological chemistry · 2009Article
- Probing the functional impact of sequence variation on p53-DNA interactions using a novel microsphere assay for protein-DNA binding with human cell extracts.PLoS genetics · 2009Article
- p53 and chemosensitivity in bladder cancer.International journal of clinical oncology · 2008Review
- Noncanonical DNA motifs as transactivation targets by wild type and mutant p53.PLoS genetics · 2008Article
- Dissecting microregulation of a master regulatory network.BMC genomics · 2008Article
- Interactions of mutant p53 with DNA: guilt by association.Oncogene · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The p53 master regulatory network provides for the stress-responsive direct control of a vast number of genes in humans that can be grouped into several biological categories including cell-cycle control, apoptosis and DNA repair. Similar to other sequence-specific master regulators, there is a matrix of key components, which provide for variation within the p53 master regulatory network that include p53 itself, target response element sequences (REs) that provide for p53 regulation of target genes, chromatin, accessory proteins and transcription machinery. Changes in any of these can impact the expression of individual genes, groups of genes and the eventual biological responses. The many REs represent the core of the master regulatory network. Since defects or altered expression of p53 are associated with over 50% of all cancers and greater than 90% of p53 mutations are in the sequence-specific DNA-binding domain, it is important to understand the relationship between wild-type or mutant p53 proteins and the target response elements. In the words of the legendary detective Sherlock Holmes, it is 'Elementary, my dear Mr. Watson'.
Indexed as
Identifiers
What OpenQuestion holds
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.