| Increase in p53 protein half-life in mouse keratinocytes following UV-B irradiation. | |
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MedLine Citation:
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PMID: 8020138 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Exposure of mammalian cells to UV radiation and other DNA-damaging agents triggers a response known as the UV response. This induction response involves a large number of genes including c-jun, cell-cycle regulatory proteins, specific repair enzymes, and the tumor suppressor gene p53. Altered expression of these genes following DNA damage is hypothesized to result in G1 arrest, thereby allowing cells to repair DNA damage prior to cell division. In the present study, we investigated expression of the p53 gene in mouse keratinocyte cell line 308 after exposure to UV-B light at a biologically relevant dose. Irradiation of 308 cells with 40 J/m2 UV-B resulted in a 4- to 10-fold induction in the level of p53 protein, peaking at 5 h post-irradiation. Northern blot analysis of RNA from UV-B irradiated cells showed no change in the steady-state level of p53 mRNA following irradiation. However, the half-life of p53 protein in UV-B irradiated 308 cells was extended approximately 7-fold, from 30 to 200 min. Additional studies were performed with specific anti-p53 monoclonal antibodies to establish whether UV-B irradiation induced a conformational change in p53 protein in irradiated cells. Metabolic labeling with 35S-methionine followed by immunoprecipitation with p53 monoclonal antibody PAb246, which recognizes the wild-type murine p53 protein, demonstrated that the p53 protein present in 308 cells possessed the wild-type conformation both before and after UV-B irradiation. In contrast, p53 antibody PAb240, which recognizes a 'conformation-dependent' epitope, was not reactive with the p53 protein present in 308 cells. Therefore, we conclude that the induction of p53 protein in mouse keratinocytes following UV-B irradiation occurred posttranscriptionally, and was due to a significant increase in p53 protein half-life. |
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Authors:
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M Liu; K R Dhanwada; D F Birt; S Hecht; J C Pelling |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Carcinogenesis Volume: 15 ISSN: 0143-3334 ISO Abbreviation: Carcinogenesis Publication Date: 1994 Jun |
Date Detail:
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Created Date: 1994-08-03 Completed Date: 1994-08-03 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 8008055 Medline TA: Carcinogenesis Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 1089-92 Citation Subset: IM |
Affiliation:
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Eppley Institute for Cancer Research, University of Nebraska Medical Center, Omaha 68198-6805. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cell Line Half-Life Keratinocytes / metabolism, radiation effects* Mice Mice, Inbred BALB C Protein Conformation RNA, Messenger / analysis Tumor Suppressor Protein p53 / chemistry, genetics, metabolism* Ultraviolet Rays |
| Grant Support | |
ID/Acronym/Agency:
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NCI CA36727-07/CA/NCI NIH HHS; NCI CA40847/CA/NCI NIH HHS; NCI K04-CA01382/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/RNA, Messenger; 0/Tumor Suppressor Protein p53 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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