| p16 and ARF: activation of teenage proteins in old age. | |
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MedLine Citation:
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PMID: 15520854 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Cellular senescence induced by different stresses and telomere shortening appears to play an important role in the aging process. The products of the INK4a/ARF locus--p16INK4a and ARF--arrest cell proliferation at the senescence stage by exerting their effects on retinoblastoma protein- and p53-mediated responsive pathways. A study in this issue of the JCI provides experimental evidence of a specific upregulation of these cell cycle inhibitors in a variety of organs during mammalian aging. |
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Authors:
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Ande Satyanarayana; K Lenhard Rudolph |
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Publication Detail:
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Type: Comment; Journal Article; Review |
Journal Detail:
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Title: The Journal of clinical investigation Volume: 114 ISSN: 0021-9738 ISO Abbreviation: J. Clin. Invest. Publication Date: 2004 Nov |
Date Detail:
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Created Date: 2004-11-02 Completed Date: 2004-12-13 Revised Date: 2009-11-18 |
Medline Journal Info:
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Nlm Unique ID: 7802877 Medline TA: J Clin Invest Country: United States |
Other Details:
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Languages: eng Pagination: 1237-40 Citation Subset: AIM; IM |
Affiliation:
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Department of Gastroenterology, Hepatology, and Endocrinology, Hannover Medical School, Hannover, Germany. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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ADP-Ribosylation Factor 1
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physiology* Aging* Animals Biological Markers Cell Aging Cyclin-Dependent Kinase Inhibitor p16 / physiology* Gene Expression Regulation Humans Models, Biological Retinoblastoma Protein / metabolism Tumor Suppressor Protein p53 / metabolism Up-Regulation |
| Chemical | |
Reg. No./Substance:
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0/Biological Markers; 0/Cyclin-Dependent Kinase Inhibitor p16; 0/Retinoblastoma Protein; 0/Tumor Suppressor Protein p53; EC 3.6.5.2/ADP-Ribosylation Factor 1 |
| Comments/Corrections | |
Comment On:
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J Clin Invest. 2004 Nov;114(9):1299-307
[PMID:
15520862
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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