ArticleNature communications2013
The p53-PUMA axis suppresses iPSC generation.
Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 58 citations in OpenAlex.
- Genes as Genome Stabilizers in Pluripotent Stem Cells.Advances in experimental medicine and biology · 2025Review
- c-Myc alone is enough to reprogram fibroblasts into functional macrophages.Journal of hematology & oncology · 2024Article
- PRPS2 mutations drive acute lymphoblastic leukemia relapse through influencing PRPS1/2 hexamer stability.Blood science (Baltimore, Md.) · 2023Article
- Fas/FasL mediates NF-κBp65/PUMA-modulated hepatocytes apoptosis via autophagy to drive liver fibrosis.Cell death & disease · 2021Article
- PUMA facilitates EMI1-promoted cytoplasmic Rad51 ubiquitination and inhibits DNA repair in stem and progenitor cells.Signal transduction and targeted therapy · 2021Article
- PRPS1-mediated purine biosynthesis is critical for pluripotent stem cell survival and stemness.Aging · 2021Article
- Cell fate, metabolic reprogramming and lncRNA of tumor-initiating stem-like cells induced by alcohol.Chemico-biological interactions · 2020Review
- Cancer Stemness: p53 at the Wheel.Frontiers in oncology · 2020Review
- A connection in life and death: The BCL-2 family coordinates mitochondrial network dynamics and stem cell fate.International review of cell and molecular biology · 2020Review
- Article
- Targeting of apoptosis gene loci by reprogramming factors leads to selective eradication of leukemia cells.Nature communications · 2019Article
- Episomal Induced Pluripotent Stem Cells: Functional and Potential Therapeutic Applications.Cell transplantation · 2019Review
- Zinc-finger protein p52-ZER6 accelerates colorectal cancer cell proliferation and tumour progression through promoting p53 ubiquitination.EBioMedicine · 2019Article
- Remodeling of mitochondrial morphology and function: an emerging hallmark of cellular reprogramming.Cell stress · 2019Review
- Cell Reprogramming in Tumorigenesis and Its Therapeutic Implications for Breast Cancer.International journal of molecular sciences · 2019Review
- Absence of cyclin-dependent kinase inhibitor p27 or p18 increases efficiency of iPSC generation without induction of iPSC genomic instability.Cell death & disease · 2019Article
- Receptor interacting protein kinase 3 (RIP3) regulates iPSCs generation through modulating cell cycle progression genes.Stem cell research · 2019Article
- A Novel Small Molecule p53 Stabilizer for Brain Cell Differentiation.Frontiers in chemistry · 2019Article
- Article
- Optimizing the method for generation of integration-free induced pluripotent stem cells from human peripheral blood.Stem cell research & therapy · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 7 institutions in 2 countries.
Funding
Abstract
Mechanisms underlying the reprogramming process of induced pluripotent stem cells remain poorly defined. Like tumorigenesis, generation of induced pluripotent stem cells was shown to be suppressed by the Trp53 (p53) pathway, at least in part via p21Cdkn1a (p21)-mediated cell cycle arrest. Here we examine the role of PUMA, a pro-apoptotic mediator of p53, during somatic reprogramming in comparison to p21 in the p53 pathway. Using mouse strains deficient in these molecules, we demonstrate that PUMA is an independent mediator of the negative effect of p53 on induced pluripotent stem cell induction. PUMA deficiency leads to a better survival rate associated with reduced DNA damage and fewer chromosomal aberrations in induced pluripotent stem cells, whereas loss of p21 or p53 results in an opposite outcome. Given these new findings, PUMA may serve as a distinct and more desirable target in the p53 pathway for induced pluripotent stem cell generation, thereby having important implications for potential therapeutic applications of induced pluripotent stem cells.
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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.