ReviewOncogene1999
The p53 gene family.
Review in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled 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.
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
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 174 citations in OpenAlex.
- Pooled it
- Review
- Molecular characterization, function, tissue differential expression, and single-nucleotide polymorphism of buffaloArchives animal breeding · 2024Article
- Review
- ΔNp63 transcript loss in bladder cancer constitutes an independent molecular predictor of TaT1 patients post-treatment relapse and progression.Journal of cancer research and clinical oncology · 2019Article
- Prognostic Impact of Melatonin Receptors MT1 and MT2 in Non-Small Cell Lung Cancer (NSCLC).Cancers · 2019Article
- Crocetin exploits p53-induced death domain (PIDD) and FAS-associated death domain (FADD) proteins to induce apoptosis in colorectal cancer.Scientific reports · 2016Article
- Oncogenic Intra-p53 Family Member Interactions in Human Cancers.Frontiers in oncology · 2016Review
- Radioprotective potential of melatonin against ⁶⁰Co γ-ray-induced testicular injury in male C57BL/6 mice.Journal of biomedical science · 2015Article
- The effect of regular exercise on development of sarcoma tumor and oxidative damage in mice liver.Journal of sports science & medicine · 2011Article
- Gain of cellular adaptation due to prolonged p53 impairment leads to functional switchover from p53 to p73 during DNA damage in acute myeloid leukemia cells.The Journal of biological chemistry · 2010Article
- Arsenic trioxide induces apoptosis in NB-4, an acute promyelocytic leukemia cell line, through up-regulation of p73 via suppression of nuclear factor kappa B-mediated inhibition of p73 transcription and prevention of NF-kappaB-mediated induction of XIAP, cIAP2, BCL-XL and survivin.Medical oncology (Northwood, London, England) · 2010Article
- NAD(P)H quinone oxidoreductase protects TAp63gamma from proteasomal degradation and regulates TAp63gamma-dependent growth arrest.PloS one · 2010Article
- Involvement of p63 in the herpes simplex virus-1-induced demise of corneal cells.Journal of biomedical science · 2010Article
- Cancer models in Caenorhabditis elegans.Developmental dynamics : an official publication of the American Association of Anatomists · 2010Review
- Targeting of p53-transcriptional dysfunction by conditionally replicating adenovirus is not limited by p53-homologues.Molecular therapy : the journal of the American Society of Gene Therapy · 2010Article
- SCH529074, a small molecule activator of mutant p53, which binds p53 DNA binding domain (DBD), restores growth-suppressive function to mutant p53 and interrupts HDM2-mediated ubiquitination of wild type p53.The Journal of biological chemistry · 2010Article
- Mutant p53 mediates survival of breast cancer cells.British journal of cancer · 2009Article
- The p53 family and programmed cell death.Oncogene · 2008Review
- Polymorphisms of TP53 Arg72Pro, but not p73 G4C14>A4TA4 and p21 Ser31Arg, contribute to risk of cutaneous melanoma.The Journal of investigative dermatology · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p73 and p63 are two recently discovered p53 homologs. Like p53, these proteins can recognize canonical p53 DNA-binding sites and, when overproduced, can activate p53-responsive target genes and induce apoptosis. Unlike p53, these genes undergo complex alternative splicing which, at least in the case of p63, yields proteins with widely divergent biological properties. In addition p73 and p63 are, in contrast to p53, rarely mutated in human cancer. Furthermore, p73 inactivation is not required for viral transformation. Thus, there is currently no firm evidence that p63 and p73 should be considered tumor suppressors. The early suggestion that monoallelic expression of p73 contributed to carcinogenesis needs to be interpreted cautiously in light of data showing interindividual and intraindividual variation with respect to monoallelic expression of p73 and the finding that p73 mRNA levels are generally increased, rather than decreased, in a host of tumors relative to normal cells.
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.