ArticleOncogene1999
Wild-type p53 protein shows calcium-dependent binding to F-actin.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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
20 citing papers in PubMed, 41 citations in OpenAlex.
- β-Actin: An Emerging Biomarker in Ischemic Stroke.Cellular and molecular neurobiology · 2023Review
- The p53 and Calcium Regulated Actin Rearrangement in Model Cells.International journal of molecular sciences · 2022Article
- β-Actin facilitates etoposide-induced p53 nuclear import.Journal of biosciences · 2020Article
- Wild-type p53 enhances endothelial barrier function by mediating RAC1 signalling and RhoA inhibition.Journal of cellular and molecular medicine · 2018Article
- The Nature of Actin-Family Proteins in Chromatin-Modifying Complexes.Frontiers in genetics · 2018Review
- Nuclear α-catenin mediates the DNA damage response via β-catenin and nuclear actin.Journal of cell science · 2017Article
- G-actin guides p53 nuclear transport: potential contribution of monomeric actin in altered localization of mutant p53.Scientific reports · 2016Article
- The actin depolymerizing factor (ADF)/cofilin signaling pathway and DNA damage responses in cancer.International journal of molecular sciences · 2015Review
- There is more than one way to model an elephant. Experiment-driven modeling of the actin cytoskeleton.Biophysical journal · 2013Review
- Actin polymerization negatively regulates p53 function by impairing its nuclear import in response to DNA damage.PloS one · 2013Article
- The nucleoskeleton as a genome-associated dynamic 'network of networks'.Nature reviews. Molecular cell biology · 2011Review
- LATS1 tumor suppressor is a novel actin-binding protein and negative regulator of actin polymerization.Cell research · 2011Article
- Mitochondrial dysfunction impairs tumor suppressor p53 expression/function.The Journal of biological chemistry · 2011Article
- Tunneling-nanotube development in astrocytes depends on p53 activation.Cell death and differentiation · 2011Article
- UFFizi: a generic platform for ranking informative features.BMC bioinformatics · 2010Article
- Relationship between serum calcium and CA 19-9 levels in colorectal cancer.World journal of gastroenterology · 2004Article
- Genomic alterations in spontaneous and carcinogen-induced murine melanoma cell lines.Oncogene · 2004Article
- Regulation of Cdc42-mediated morphological effects: a novel function for p53.The EMBO journal · 2002Article
- The interaction of p53 with the nuclear matrix is mediated by F-actin and modulated by DNA damage.Oncogene · 2002Article
- p53 regulation by post-translational modification and nuclear retention in response to diverse stresses.Oncogene · 1999Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear localization of p53 is required for p53 to detect and respond to DNA strand abnormalities and breaks following DNA damage. This leads to activation of the tumour suppressive functions of p53 resulting in either cell cycle arrest and DNA repair; or apoptosis. Critical functional changes in DNA which require strand breaks, including gene rearrangement, may transiently mimic DNA damage: here it is important not to trigger a p53 response. The fine control of p53 in these different circumstances is unknown but may include transient sequestering of p53 in the cytoplasm. Reversible nuclear-cytoplasmic shuttling is an intrinsic property of p53 (Middeler et al., 1997) associated with cell cycle-related changes in p53's subcellular distribution. Takahashi and Suzuki (1994) described p53 inactivation by shuttling to the cytoplasm and Katsumoto et al. (1995) found wild-type p53 to be closely associated with cytoplasmic actin filaments during DNA synthesis. Here we show that, in the presence of free calcium ions, p53 binds directly to F-actin with a dissocation constant of about 10 microM. Thus, part of the regulatory machinery in normal cell cycling may involve p53-actin interactions regulated by calcium fluxes and the dynamic turnover of F-actin.
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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.