| E2F1 works as a cell cycle suppressor in mature neurons. | |
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MedLine Citation:
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PMID: 18003834 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Neurons are highly differentiated cells that normally never enter a cell cycle; if they do, the result is usually death, not division. For example, cerebellar granule neurons in staggerer and lurcher mutant mice initiate a cell cycle-like process just before they die. E2F1 is a transcription factor that promotes cell cycle progression. Because E2F1 is also involved in apoptosis, we bred double mutants (E2f1-/-; staggerer and E2f1-/-; lurcher) to assess its role in the cell cycle-related death of cerebellar granule cells in vivo. We found neither granule cell cycle initiation nor cell death was significantly altered in either double mutant. However, after postnatal day 10, neurons throughout the CNS of E2f1-/- and E2f1+/- animals were found to express cell cycle proteins and replicate their DNA. Whereas Map2 and synapsin1 staining are little altered, there is a reduction of calbindin in Purkinje cell dendrites at 1 year of age, suggesting that the mutant cells also undergo a slow, subtle atrophy. These events are cell autonomous, because cultured E2f1-/- cortical neurons "cycle" in vitro, whereas wild-type neurons do not. Our results suggest that, in mature CNS neurons, E2F1 functions as a cell cycle suppressor. |
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Authors:
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Li Wang; Rong Wang; Karl Herrup |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: The Journal of neuroscience : the official journal of the Society for Neuroscience Volume: 27 ISSN: 1529-2401 ISO Abbreviation: J. Neurosci. Publication Date: 2007 Nov |
Date Detail:
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Created Date: 2007-11-16 Completed Date: 2007-12-19 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8102140 Medline TA: J Neurosci Country: United States |
Other Details:
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Languages: eng Pagination: 12555-64 Citation Subset: IM |
Affiliation:
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Department of Genetics, Case Western Reserve University School of Medicine, Cleveland, Ohio 44120, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / genetics* Calcium-Binding Protein, Vitamin D-Dependent / metabolism Cell Aging / genetics Cell Cycle / genetics Cell Cycle Proteins / genetics, physiology* Cell Differentiation / genetics Cerebellum / growth & development*, metabolism*, physiopathology Cyclin A / genetics, metabolism DNA Replication / genetics E2F1 Transcription Factor / genetics, physiology* Female Male Mice Mice, Inbred C57BL Mice, Knockout Mutation / genetics Neurons / metabolism*, pathology Proliferating Cell Nuclear Antigen / genetics, metabolism |
| Grant Support | |
ID/Acronym/Agency:
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P50-AG08012/AG/NIA NIH HHS; R01-AG24494/AG/NIA NIH HHS; R01-NS20591/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Calcium-Binding Protein, Vitamin D-Dependent; 0/Cell Cycle Proteins; 0/Cyclin A; 0/E2F1 Transcription Factor; 0/E2f1 protein, mouse; 0/Proliferating Cell Nuclear Antigen; 0/calbindin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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