ArticleThe Journal of cell biology1996
Induction of DNA synthesis and apoptosis in cardiac myocytes by E1A oncoprotein.
Article in The Journal of cell biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 95 citations in OpenAlex.
- Cyclin A2 induces cytokinesis in human adult cardiomyocytes and drives reprogramming in mice.NPJ Regenerative medicine · 2025Article
- Regulation of Cardiomyocyte Division During Cardiac Regeneration.Current cardiology reports · 2023Review
- Molecular mechanisms of heart regeneration.Seminars in cell & developmental biology · 2020Review
- Mechanisms of Cardiomyocyte Proliferation and Differentiation in Development and Regeneration.Current cardiology reports · 2017Review
- Cardiac regeneration based on mechanisms of cardiomyocyte proliferation and differentiation.Stem cell research · 2014Review
- Binucleation of cardiomyocytes: the transition from a proliferative to a terminally differentiated state.Drug discovery today · 2014Review
- Enhanced proliferation of monolayer cultures of embryonic stem (ES) cell-derived cardiomyocytes following acute loss of retinoblastoma.PloS one · 2008Article
- Cardiac myocyte cell cycle control in development, disease, and regeneration.Physiological reviews · 2007Review
- Adenoviral delivery of human CDC5 promotes G2/M progression and cell division in neonatal ventricular cardiomyocytes.Gene therapy · 2006Article
- Phosphorylation-dependent degradation of p300 by doxorubicin-activated p38 mitogen-activated protein kinase in cardiac cells.Molecular and cellular biology · 2005Article
- Caspase inhibition protects against reovirus-induced myocardial injury in vitro and in vivo.Journal of virology · 2004Article
- Repression of c-Myc and inhibition of G1 exit in cells conditionally overexpressing p300 that is not dependent on its histone acetyltransferase activity.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Cell cycle regulation to repair the infarcted myocardium.Heart failure reviews · 2003Review
- p21(CIP1) Controls proliferating cell nuclear antigen level in adult cardiomyocytes.Molecular and cellular biology · 2003Article
- Transgenic expression in mouse lung reveals distinct biological roles for the adenovirus type 5 E1A 243- and 289-amino-acid proteins.Journal of virology · 2002Article
- Reconstitution of cyclin D1-associated kinase activity drives terminally differentiated cells into the cell cycle.Molecular and cellular biology · 2001Article
- Antisense-mediated depletion of p300 in human cells leads to premature G1 exit and up-regulation of c-MYC.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- A novel Rb- and p300-binding protein inhibits transactivation by MyoD.Molecular and cellular biology · 2000Article
- Involvement of retinoblastoma family members and E2F/DP complexes in the death of neurons evoked by DNA damage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- Cell cycle withdrawal promotes myogenic induction of Akt, a positive modulator of myocyte survival.Molecular and cellular biology · 1999Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Beginning during the second half of gestation, increasing numbers of cardiac myocytes withdraw from the cell cycle such that DNA synthesis is no longer detectable in these cells by neonatal day 17 in vivo. The mechanisms that exclude these and other terminally differentiated cells from the cell division cycle are poorly understood. To begin to explore the molecular basis of the barrier to G1/S progression in cardiac myocytes, we used adenoviruses to express wild-type and mutant E1A proteins in primary cultures from embryonic day 20 rats. While most of these cardiac myocytes are ordinarily refractory to DNA synthesis, even in the presence of serum growth factors, expression of wild-type E1A stimulates DNA synthesis in up to 94% or almost all successfully transduced cells. Rather than complete the cell cycle, however, these cells undergo apoptosis. Apoptosis is limited to those cells that engage in DNA synthesis, and the kinetics of the two processes suggest that DNA synthesis precedes apoptosis. Mutations in E1A that disable it from binding Rb and related pocket proteins have little effect on its ability to stimulate DNA synthesis in cardiac myocytes. In contrast, mutants that are defective in binding the cellular protein p300 stimulate DNA synthesis 2.4-4.1-fold less efficiently, even in the context of retained E1A pocket protein binding. In the absence of ElA pocket protein binding, the usual situation in the cell, loss of p300 binding severely decreases the ability of ElA to stimulate DNA synthesis. These results suggest that the barrier to G1/S progression in cardiac myocytes is mediated. at least in part, by the same molecules that gate the G1/S transition in actively cycling cells, and that p300 or related family members play an important role in this process.
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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.