ArticlePloS one2018
Atypical E2f functions are critical for pancreas polyploidization.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Integrating the Study of Polyploidy Across Organisms, Tissues, and Disease.Annual review of genetics · 2024Review
- Binucleated human hepatocytes arise through late cytokinetic regression during endomitosis M phase.The Journal of cell biology · 2024Article
- Origins of cancer: ain't it just mature cells misbehaving?The EMBO journal · 2024Review
- Functional consequences of somatic polyploidy in development.Development (Cambridge, England) · 2024Review
- Cellular polyploidy in organ homeostasis and regeneration.Protein & cell · 2023Article
- Wnt signaling regulates hepatocyte cell division by a transcriptional repressor cascade.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Cell Cycle Re-entry in the Nervous System: From Polyploidy to Neurodegeneration.Frontiers in cell and developmental biology · 2021Review
- The broken cycle: E2F dysfunction in cancer.Nature reviews. Cancer · 2019Review
- Solving the Polyploid Mystery in Health and Disease.Trends in genetics : TIG · 2019Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The presence of polyploid cells in the endocrine and exocrine pancreas has been reported for four decades. In rodents, pancreatic polyploidization is initiated after weaning and the number of polyploid cells increases with age. Surprisingly the molecular regulators and biological functions of polyploidization in the pancreas are still unknown. We discovered that atypical E2f activity is essential for polyploidization in the pancreas, using an inducible Cre/LoxP approach in new-born mice to delete ubiquitously the atypical E2f transcription factors, E2f7 and E2f8. In contrast to its critical role in embryonic survival, conditional deletion of both of both atypical E2fs in newborn mice had no impact on postnatal survival and mice lived until old age. However, deficiency of E2f7 or E2f8 alone was sufficient to suppress polyploidization in the pancreas and associated with only a minor decrease in blood serum levels of glucose, insulin, amylase and lipase under 4 hours starvation condition compared to wildtype littermates. In mice with fewer pancreatic polyploid cells that were fed ad libitum, no major impact on hormones or enzymes levels was observed. In summary, we identified atypical E2fs to be essential for polyploidization in the pancreas and discovered that postnatal induced loss of both atypical E2fs in many organs is compatible with life until old age.
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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.