ArticleCell death & disease2010
p73 deficiency results in impaired self renewal and premature neuronal differentiation of mouse neural progenitors independently of p53.
Article in Cell death & disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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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.
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Who cites it
46 citing papers in PubMed, 58 citations in OpenAlex.
- Safely Targeting Cancer, the Wound That Never Heals, Utilizing CBP/Beta-Catenin Antagonists.Cancers · 2025Article
- A novel TAp73-inhibitory compound counteracts stemness features of glioblastoma stem cells.Molecular oncology · 2025Article
- Mouse cortical organoids reveal key functions of p73 isoforms: TAp73 governs the establishment of the archetypical ventricular-like zones while DNp73 is central in the regulation of neural cell fate.Frontiers in cell and developmental biology · 2024Article
- Single-cell transcriptome atlas of human mesenchymal stem cells exploring cellular heterogeneity.Clinical and translational medicine · 2021Article
- Deciphering the Nature ofCancers · 2021Article
- p73 as a Tissue Architect.Frontiers in cell and developmental biology · 2021Review
- Regulation of Adult Neurogenesis in Mammalian Brain.International journal of molecular sciences · 2020Review
- p53-Related Transcription Targets of TAp73 in Cancer Cells-Bona Fide or Distorted Reality?International journal of molecular sciences · 2020Review
- Tissue-specific roles of p73 in development and homeostasis.Journal of cell science · 2019Review
- Cajal-Retzius neurons are required for the development of the human hippocampal fissure.Journal of anatomy · 2019Article
- Article
- TheFrontiers in genetics · 2019Review
- p73 Regulates Primary Cortical Neuron Metabolism: a Global Metabolic Profile.Molecular neurobiology · 2018Article
- Non-oncogenic roles of TAp73: from multiciliogenesis to metabolism.Cell death and differentiation · 2018Review
- "Till Death Do Us Part": A Potential Irreversible Link Between Aberrant Cell Cycle Control and Neurodegeneration in the Adult Olfactory Bulb.Frontiers in neuroscience · 2018Review
- p73 is required for appropriate BMP-induced mesenchymal-to-epithelial transition during somatic cell reprogramming.Cell death & disease · 2017Article
- Expression of the Parkinson's Disease-Associated Gene Alpha-Synuclein is Regulated by the Neuronal Cell Fate Determinant TRIM32.Molecular neurobiology · 2017Article
- De novo missense variants in HECW2 are associated with neurodevelopmental delay and hypotonia.Journal of medical genetics · 2017Article
- Combinatorial identification of DNA methylation patterns over age in the human brain.BMC bioinformatics · 2016Article
- How Does p73 Cause Neuronal Defects?Molecular neurobiology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The question of how neural progenitor cells maintain its self-renewal throughout life is a fundamental problem in cell biology with implications in cancer, aging and neurodegenerative diseases. In this work, we have analyzed the p73 function in embryonic neural progenitor cell biology using the neurosphere (NS)-assay and showed that p73-loss has a significant role in the maintenance of neurosphere-forming cells in the embryonic brain. A comparative study of NS from Trp73-/-, p53KO, p53KO;Trp73-/- and their wild-type counterparts demonstrated that p73 deficiency results in two independent, but related, phenotypes: a smaller NS size (related to the proliferation and survival of the neural-progenitors) and a decreased capacity to form NS (self-renewal). The former seems to be the result of p53 compensatory activity, whereas the latter is p53 independent. We also demonstrate that p73 deficiency increases the population of neuronal progenitors ready to differentiate into neurons at the expense of depleting the pool of undifferentiated neurosphere-forming cells. Analysis of the neurogenic niches demonstrated that p73-loss depletes the number of neural-progenitor cells, rendering deficient niches in the adult mice. Altogether, our study identifies TP73 as a positive regulator of self-renewal with a role in the maintenance of the neurogenic capacity. Thus, proposing p73 as an important player in the development of neurodegenerative diseases and a potential therapeutic target.
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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.