ReviewCell cycle (Georgetown, Tex.)2010
Removing all obstacles: a critical role for p53 in promoting tissue renewal.
Review in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 31 citations in OpenAlex.
- Sequential drug release from dual-responsive scaffold with ultrasound-enhanced efficacy for infectious oral ulcer therapy.Regenerative biomaterials · 2026Article
- Role of Dietary Antioxidants in p53-Mediated Cancer Chemoprevention and Tumor Suppression.Oxidative medicine and cellular longevity · 2021Review
- The p53/Adipose-Tissue/Cancer Nexus.Frontiers in endocrinology · 2018Review
- Regulation of kidney development by the Mdm2/Mdm4-p53 axis.Journal of molecular cell biology · 2017Review
- The Paradox of p53: What, How, and Why?Cold Spring Harbor perspectives in medicine · 2016Review
- Down-regulation of LATS kinases alters p53 to promote cell migration.Genes & development · 2015Article
- p53 Enables metabolic fitness and self-renewal of nephron progenitor cells.Development (Cambridge, England) · 2015Article
- Role of tumor suppressor genes in the cancer-associated reprogramming of human induced pluripotent stem cells.Stem cell research & therapy · 2014Review
- Rapamycin induces pluripotent genes associated with avoidance of replicative senescence.Cell cycle (Georgetown, Tex.) · 2013Article
- Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy.International journal of molecular sciences · 2013Article
- Mechanisms that regulate stem cell aging and life span.Cell stem cell · 2013Review
- Cdkn1b overexpression in adult mice alters the balance between genome and tissue ageing.Nature communications · 2013Article
- Loss of p53 exacerbates multiple myeloma phenotype by facilitating the reprogramming of hematopoietic stem/progenitor cells to malignant plasma cells by MafB.Cell cycle (Georgetown, Tex.) · 2012Article
- Genotoxic exposure during juvenile growth of mammary gland depletes stem cell activity and inhibits Wnt signaling.PloS one · 2012Article
- Oncogenic stress sensitizes murine cancers to hypomorphic suppression of ATR.The Journal of clinical investigation · 2012Article
- Targeting the p53 signaling pathway in cancer therapy - the promises, challenges and perils.Expert opinion on therapeutic targets · 2012Review
- Cooperative effects of Akt-1 and Raf-1 on the induction of cellular senescence in doxorubicin or tamoxifen treated breast cancer cells.Oncotarget · 2011Article
- The role of p21 in regulating mammalian regeneration.Stem cell research & therapy · 2011Article
- Article
- p53 prevents progression of nevi to melanoma predominantly through cell cycle regulation.Pigment cell & melanoma research · 2010Article
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 2 countries.
Funding
Abstract
Defects in DNA repair pathways or exposure to high levels of DNA damaging agents limit the renewal potential of adult tissues and accelerate the development of age-related degenerative pathologies. Many studies suggest these tissue homeostatic defects can result from the accumulation of DNA damage in tissue-specific stem cells. Although maintenance of genome integrity in progenitor cells is required for the renewal of adult tissues, recent studies have highlighted the importance of additional mechanisms that facilitate and direct the process of tissue regeneration. These reports indicate that the p53 tumor suppressor gene maintains adult tissue homeostasis and promotes tissue renewal by suppressing the accumulation of DNA-damaged cells. Without p53, tissue deterioration caused by the elimination of genome maintenance regulators (ATR, Hus1 or Terc) is exacerbated and, in some cases, leads to synthetic lethality at the organismal level. Importantly, the accumulation of highly damaged cells in multiple tissues appears to severely impede regeneration from undamaged progenitors, suggesting that p53-mediated removal of damaged cells is a prerequisite for efficient progenitor driven renewal. These findings argue that tissue homeostasis is governed not only by the intrinsic repopulating potential of competent progenitors, but also by mechanisms that limit the accumulation of defective cells and, thereby, promote compensatory regeneration. As discussed in this review, these findings advance our understanding of mechanisms that counter the effects of DNA damage at the tissue level and have important implications for the development of therapeutic approaches to combating age-related pathologies and p53-deficient malignancies.
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.