| Inducing cellular senescence using defined genetic elements. | |
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MedLine Citation:
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PMID: 17634581 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Cellular senescence is generally defined as an irreversible state of G1 cell cycle arrest in which cells are refractory to growth factor stimulation. Cellular senescence can be induced through several different mechanisms. Primary mammalian cells display a finite life span, suggesting a mechanism that counts cell divisions. Those cells initially proliferate but eventually enter a state of permanent growth arrest, called replicative senescence. Erosion of telomeric DNA has emerged as a key factor in replicative senescence, which is antagonized during cell immortalization. Nevertheless, besides telomere shortening, there are other mechanisms inducing a growth arrest similar to the replicative senescencent phenotype. Oncogenic or mitogenic signals as well as DNA damage can induce such a phenotype of cellular senescence. All forms of cellular senescence share common signaling pathways and morphological features. Thereby, p53 seems to be essential for the senescence response. Many of these senescence inducing mechanisms can be experimentally recapitulated by the introduction of defined genetic elements. Replicative senescence due to telomere shortening can, for example, be induced by a dominant negative version of telomerase, premature senescence by the overexpression of oncogenic ras, or p16. |
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Authors:
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Hiroshi Nakagawa; Oliver G Opitz |
Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Methods in molecular biology (Clifton, N.J.) Volume: 371 ISSN: 1064-3745 ISO Abbreviation: Methods Mol. Biol. Publication Date: 2007 |
Date Detail:
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Created Date: 2007-07-19 Completed Date: 2007-09-21 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9214969 Medline TA: Methods Mol Biol Country: United States |
Other Details:
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Languages: eng Pagination: 167-78 Citation Subset: IM |
Affiliation:
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Gastroenterology Division, Department of Medicine and Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cell Aging / genetics* Cells, Cultured Cyclin-Dependent Kinase Inhibitor p16 / genetics* DNA Damage / genetics* G1 Phase / genetics* Genes, ras / genetics* Humans Mice Signal Transduction / genetics Telomere / genetics Tumor Suppressor Protein p53 / genetics* |
| Chemical | |
Reg. No./Substance:
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0/Cyclin-Dependent Kinase Inhibitor p16; 0/Tumor Suppressor Protein p53 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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