ArticleOncogene1999
The role of wild-type p53 in the differentiation of primary hemopoietic and muscle cells.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Pooled it
- Individually tailored screening of susceptibility to sarcopenia using p53 codon 72 polymorphism, phenotypes, and conventional risk factors.Disease markers · 2014Trial
- Establishment and characterization of a skeletal myoblast cell line of grass carp (Ctenopharyngodon idellus).Fish physiology and biochemistry · 2023Article
- The association between TP53 rs1625895 polymorphism and the risk of sarcopenic obesity in Iranian older adults: a case-control study.BMC musculoskeletal disorders · 2021Article
- Epigenetically modified cardiac mesenchymal stromal cells limit myocardial fibrosis and promote functional recovery in a model of chronic ischemic cardiomyopathy.Basic research in cardiology · 2018Article
- The Epigenetic Regulator HDAC1 Modulates Transcription of a Core Cardiogenic Program in Human Cardiac Mesenchymal Stromal Cells Through a p53-Dependent Mechanism.Stem cells (Dayton, Ohio) · 2016Article
- P53 functional abnormality in mesenchymal stem cells promotes osteosarcoma development.Cell death & disease · 2016Review
- Malat1 as an evolutionarily conserved lncRNA, plays a positive role in regulating proliferation and maintaining undifferentiated status of early-stage hematopoietic cells.BMC genomics · 2015Article
- Cell Differentiation and Checkpoint.International journal of cancer research and molecular mechanisms · 2015Article
- Kras activation in p53-deficient myoblasts results in high-grade sarcoma formation with impaired myogenic differentiation.Oncotarget · 2015Article
- A differential response to newt regeneration extract by C2C12 and primary mammalian muscle cells.Skeletal muscle · 2015Article
- Article
- Regulation of p53 is critical for vertebrate limb regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- p53 and MDM2 are involved in the regulation of osteocalcin gene expression.Experimental cell research · 2012Article
- HIPK2 is involved in cell proliferation and its suppression promotes growth arrest independently of DNA damage.Cell proliferation · 2009Article
- Wild-type p53 gene transfer is not detrimental to normal cells in vivo: implications for tumor gene therapy.Oncogene · 2004Article
- Immortalization of mouse myogenic cells can occur without loss of p16INK4a, p19ARF, or p53 and is accelerated by inactivation of Bax.BMC cell biology · 2004Article
- p53 regulates myogenesis by triggering the differentiation activity of pRb.The Journal of cell biology · 2000Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Experiments previously performed on 32D and C2C12 cell lines indicated that wild type p53 (wtp53) protein has a role in granulocyte and myotube differentiation. Since these are immortal cells, we asked whether the inhibition of differentiation induced by the expression of dominant-negative p53 (dnp53) proteins was dependent on the immortalization-determined microenvironment. Thus, we evaluated the effects produced by interfering with the endogenous p53 gene in murine primary hemopoietic and muscle cells. Expression of dnp53 protein reduced the differentiation of bone marrow cells into granulocytes and macrophages. Moreover, p53 activation was measurable during the differentiation process of primary myoblasts, while interference with this activation led to a consistent slow down of terminal differentiation. Since the impairment of the differentiation was not accompanied by alterations in the cell cycle withdrawal and in the rate of apoptosis which are coupled with these types of differentiation, the data here reported support a specific role for p53 in the differentiation process. However, the difference in the intensity of inhibition between immortal and primary cells, i. e., complete versus slow down, respectively, suggests that the immortalization process might render the cells more sensitive to the loss of wtp53 activity for the differentiation process.
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.