ArticleThe Journal of cell biology2000
Subcellular compartmentalization of E2F family members is required for maintenance of the postmitotic state in terminally differentiated muscle.
Article in The Journal of cell biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 43 citations in OpenAlex.
- E2F4DN Transgenic Mice: A Tool for the Evaluation of E2F4 as a Therapeutic Target in Neuropathology and Brain Aging.International journal of molecular sciences · 2022Review
- E2F4 transcription factor is a prognostic biomarker related to immune infiltration of head and neck squamous cell carcinoma.Scientific reports · 2022Article
- A non canonical subtilase attenuates the transcriptional activation of defence responses ineLife · 2016Article
- Diabetes mellitus--advances and challenges in human β-cell proliferation.Nature reviews. Endocrinology · 2015Review
- Targeted gene mutation of E2F1 evokes age-dependent synaptic disruption and behavioral deficits.Journal of neurochemistry · 2014Article
- ERK-associated changes in E2F4 phosphorylation, localization and transcriptional activity during mitogenic stimulation in human intestinal epithelial crypt cells.BMC cell biology · 2013Article
- Human pancreatic β-cell G1/S molecule cell cycle atlas.Diabetes · 2013Article
- CMF1-Rb interaction promotes myogenesis in avian skeletal myoblasts.Developmental dynamics : an official publication of the American Association of Anatomists · 2008Article
- Location, location, location: altered transcription factor trafficking in neurodegeneration.Journal of neuropathology and experimental neurology · 2007Review
- Rb-mediated neuronal differentiation through cell-cycle-independent regulation of E2f3a.PLoS biology · 2007Article
- Activation of p38- and CRM1-dependent nuclear export promotes E2F1 degradation during keratinocyte differentiation.Oncogene · 2007Article
- MyoD synergizes with the E-protein HEB beta to induce myogenic differentiation.Molecular and cellular biology · 2006Article
- Coupling of caspase-9 to Apaf1 in response to loss of pRb or cytotoxic drugs is cell-type-specific.The EMBO journal · 2004Article
- Nucleocytoplasmic shuttling of p130/RBL2: novel regulatory mechanism.Molecular and cellular biology · 2002Article
- E2F2 converts reversibly differentiated PC12 cells to an irreversible, neurotrophin-dependent state.Oncogene · 2001Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maintenance of cells in a quiescent state after terminal differentiation occurs through a number of mechanisms that regulate the activity of the E2F family of transcription factors. We report here that changes in the subcellular compartmentalization of the E2F family proteins are required to prevent nuclei in terminally differentiated skeletal muscle from reentering S phase. In terminally differentiated L6 myotubes, E2F-1, E2F-3, and E2F-5 were primarily cytoplasmic, E2F-2 was nuclear, whereas E2F-4 became partitioned between both compartments. In these same cells, pRB family members, pRB, p107, and p130 were also nuclear. This compartmentalization of the E2F-1 and E2F-4 in differentiated muscle cells grown in vitro reflected their observed subcellular location in situ. We determined further that exogenous E2F-1 or E2F-4 expressed in myotubes at levels fourfold greater than endogenous proteins compartmentalized identically to their endogenous counterparts. Only when overexpressed at higher levels was inappropriate subcellular location for these proteins observed. At these levels, induction of the E2F-regulated genes, cyclins A and E, and suppression of factors associated with myogenesis, myogenin, and p21(Cip1) was observed. Only at these levels of E2F expression did nuclei in these terminally differentiated cells enter S phase. These data demonstrate that regulation of the subcellular compartmentalization of E2F-family members is required to maintain nuclei in a quiescent state in terminally differentiated cells.
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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.