A collection of research articles explores developments in interfacial transport and mixing, with wide-ranging practical applications.
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Edited by Bert Vogelstein, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD (received for review April 10, 2003)
Abstract
Exposure to short-wavelength UV light (UVC) strongly induces p53 expression. In human RKO colorectal carcinoma cells, this increase was not due to elevated p53 mRNA abundance, cytoplasmic export of p53 mRNA, or UVC-triggered stabilization of the p53 protein. Instead, p53 translation was potently enhanced after UVC irradiation. The 3′ UTR of p53 was found to be a target of the RNA-binding protein HuR in a UVC-dependent manner in vitro and in vivo. HuR-overexpressing RKO cells displayed elevated p53 levels, whereas cells expressing reduced HuR showed markedly diminished p53 abundance and p53 translation. Our results demonstrate a role for HuR in binding to the p53 mRNA and enhancing its translation.
Footnotes
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↵‡ To whom correspondence should be addressed at: Box 12, Laboratory of Cellular and Molecular Biology, National Institute on Aging–Intramural Research Program, National Institutes of Health, 5600 Nathan Shock Drive, Baltimore, MD 21224. E-mail: myriam-gorospe{at}nih.gov.
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This paper was submitted directly (Track II) to the PNAS office.
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Abbreviations: ELAV, embryonic lethal abnormal vision; UVC, short-wavelength UV light; REMSA, RNA electrophoretic mobility-shift assay; IP, immunoprecipitation; siRNA, small interfering RNA; CR, coding region.
- Received April 10, 2003.
- Accepted May 19, 2003.
- Copyright © 2003, The National Academy of Sciences
- Krystyna Mazan-Mamczarz*,
- Stefanie Galbán*,
- Isabel López de Silanes*,
- Jennifer L. Martindale*,
- Ulus Atasoy†,
- Jack D. Keene†, and
- Myriam Gorospe *‡
- *Laboratory of Cellular and Molecular Biology, National Institute on Aging–Intramural Research Program, National Institutes of Health, Baltimore, MD 21224; and †Duke University School of Medicine, Durham, NC 27710
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Edited by Bert Vogelstein, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD (received for review April 10, 2003)
Abstract
Exposure to short-wavelength UV light (UVC) strongly induces p53 expression. In human RKO colorectal carcinoma cells, this increase was not due to elevated p53 mRNA abundance, cytoplasmic export of p53 mRNA, or UVC-triggered stabilization of the p53 protein. Instead, p53 translation was potently enhanced after UVC irradiation. The 3′ UTR of p53 was found to be a target of the RNA-binding protein HuR in a UVC-dependent manner in vitro and in vivo. HuR-overexpressing RKO cells displayed elevated p53 levels, whereas cells expressing reduced HuR showed markedly diminished p53 abundance and p53 translation. Our results demonstrate a role for HuR in binding to the p53 mRNA and enhancing its translation.
- UV light
- embryonic lethal abnormal vision
Footnotes
-
↵‡ To whom correspondence should be addressed at: Box 12, Laboratory of Cellular and Molecular Biology, National Institute on Aging–Intramural Research Program, National Institutes of Health, 5600 Nathan Shock Drive, Baltimore, MD 21224. E-mail: myriam-gorospe{at}nih.gov.
-
This paper was submitted directly (Track II) to the PNAS office.
-
Abbreviations: ELAV, embryonic lethal abnormal vision; UVC, short-wavelength UV light; REMSA, RNA electrophoretic mobility-shift assay; IP, immunoprecipitation; siRNA, small interfering RNA; CR, coding region.
- Received April 10, 2003.
- Accepted May 19, 2003.
- Copyright © 2003, The National Academy of Sciences
RNA-binding protein HuR enhances p53 translation in response to ultraviolet light irradiation
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