ReviewMedical molecular morphology2006
Posttranslational phosphorylation of mutant p53 protein in tumor development.
Review in Medical molecular morphology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 48 citations in OpenAlex.
- From regulation to deregulation of p53 in hematologic malignancies: implications for diagnosis, prognosis and therapy.Biomarker research · 2024Review
- Molecular insights and clinical implications for the tumor suppressor role of SCFBiochimica et biophysica acta. Reviews on cancer · 2024Review
- Clinical significance of FBXW7 loss of function in human cancers.Molecular cancer · 2022Review
- Cancer-Associated Mutations Perturb the Disordered Ensemble and Interactions of the Intrinsically Disordered p53 Transactivation Domain.Journal of molecular biology · 2021Article
- Immunohistochemical detection of p53 and pp53 SerBMC veterinary research · 2020Article
- Therapeutic potential of ReACp53 targeting mutant p53 protein in CRPC.Prostate cancer and prostatic diseases · 2020Article
- Age-dependent copy number variations of TP53 tumour suppressor gene associated with altered phosphorylation status of p53 protein in sporadic schwannomas.Journal of neuro-oncology · 2019Article
- Regulators of Oncogenic Mutant TP53 Gain of Function.Cancers · 2018Review
- Tumor suppressive role for kinases phosphorylating p53 in DNA damage-induced apoptosis.Cancer science · 2018Review
- Mycobacteria Manipulate G-Protein-Coupled Receptors to Increase Mucosal Rac1 Expression in the Lungs.Journal of innate immunity · 2017Article
- Leucine-Rich Repeat Kinase 2 (LRRK2) phosphorylates p53 and induces p21(WAF1/CIP1) expression.Molecular brain · 2015Article
- FBXW7-mutated colorectal cancer cells exhibit aberrant expression of phosphorylated-p53 at Serine-15.Oncotarget · 2015Article
- Evolutionary Action Score of TP53 Coding Variants Is Predictive of Platinum Response in Head and Neck Cancer Patients.Cancer research · 2015Article
- Modelling the p53/p66Shc Aging Pathway in the Shortest Living Vertebrate Nothobranchius Furzeri.Aging and disease · 2015Review
- Bioinformatics study of cancer-related mutations within p53 phosphorylation site motifs.International journal of molecular sciences · 2014Article
- Mutant TP53 posttranslational modifications: challenges and opportunities.Human mutation · 2014Review
- Nutlin-3 downregulates p53 phosphorylation on serine392 and induces apoptosis in hepatocellular carcinoma cells.BMB reports · 2014Article
- p53 mutations in cancer.Nature cell biology · 2013Review
- Met acts through Abl to regulate p53 transcriptional outcomes and cell survival in the developing liver.Journal of hepatology · 2012Article
- The rebel angel: mutant p53 as the driving oncogene in breast cancer.Carcinogenesis · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p53 has been called the "cellular gatekeeper" and the "genome guard," because in response to exposure to DNA-damaging agents, it induces cell-cycle arrest in G1 or apoptosis and also directly affects DNA replication. Multiple mechanisms regulate p53 activity and posttranslational modification, including multisite phosphorylation of wild-type p53, in particular. Normal functions of wild-type p53 are abrogated by mutation of this gene, and oncogenic studies have revealed that p53 mutation is among the most common genetic alteration in human cancers. It is generally accepted that mutant p53 protein may not only lose the tumor suppressor functions of wild-type p53 but also acquire additional tumorigenetic roles, including dominant-negative effects and gain of function. Although many studies have revealed such aberrant functions of mutant p53, less is known about the posttranslational phosphorylation status of mutant p53 and novel biological functions of phosphorylation in carcinogenesis.
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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.