ReviewInternational journal of molecular sciences2019
Regulation of the p53 Family Proteins by the Ubiquitin Proteasomal Pathway.
Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- Pooled it
- Fgl2-knockout tumor cells serve as a vaccine inducing long-duration brain-resident memory T cells that reject subsequent intracranial tumor cell challenges.Cancer letters · 2026Article
- RBBP6 and cancer: from molecular mechanisms to clinical implications.Frontiers in oncology · 2026Review
- Effect ofPharmaceuticals (Basel, Switzerland) · 2025Article
- Article
- Melatonin mitigates ovarian aging through regulation of the YTHDF2/mActa biochimica et biophysica Sinica · 2025Article
- Ferroptosis as a therapeutic vulnerability in MDM2 inhibition in dedifferentiated liposarcoma.Oncology letters · 2025Article
- Deciphering UBE4B phosphorylation dynamics: a key mechanism in p53 accumulation and cancer cell response to DNA damage.Cell death discovery · 2025Article
- Side-stepping the guardian of the genome: current cancer therapeutics targeting mutant p53.Frontiers in pharmacology · 2025Review
- TIP60 enhances cisplatin resistance via regulating ΔNp63α acetylation in SCC.Cell death & disease · 2024Article
- Re-appraising the evidence for the source, regulation and function of p53-family isoforms.Nucleic acids research · 2024Review
- UBE2C promotes LUAD progression by ubiquitin-dependent degradation of p53 to inactivate the p53/p21 signaling pathway.Discover oncology · 2024Article
- Turmeric-Black Cumin Essential Oils and Their Capacity to Attenuate Free Radicals, Protein Denaturation, and Cancer Proliferation.Molecules (Basel, Switzerland) · 2024Article
- Unlocking the Gateway: The Spatio-Temporal Dynamics of the p53 Family Driven by the Nuclear Pores and Its Implication for the Therapeutic Approach in Cancer.International journal of molecular sciences · 2024Review
- Selectively advantageous instability in biotic and pre-biotic systems and implications for evolution and aging.Frontiers in aging · 2024Review
- Ribosome Biogenesis and Cancer: Insights into NOB1 and PNO1 Mechanisms.Current pharmaceutical design · 2024Review
- Article
- Article
- Article
- Regulation of Oocyte Apoptosis: A View from Gene Knockout Mice.International journal of molecular sciences · 2023Review
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 1 institution in 1 country.
Funding
Abstract
The tumor suppressor p53 and its homologues, p63 and p73, play a pivotal role in the regulation of the DNA damage response, cellular homeostasis, development, aging, and metabolism. A number of mouse studies have shown that a genetic defect in the p53 family could lead to spontaneous tumor development, embryonic lethality, or severe tissue abnormality, indicating that the activity of the p53 family must be tightly regulated to maintain normal cellular functions. While the p53 family members are regulated at the level of gene expression as well as post-translational modification, they are also controlled at the level of protein stability through the ubiquitin proteasomal pathway. Over the last 20 years, many ubiquitin E3 ligases have been discovered that directly promote protein degradation of p53, p63, and p73 in vitro and in vivo. Here, we provide an overview of such E3 ligases and discuss their roles and functions.
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.