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- Anne-Laure Pauleau
- Department of Infectious Diseases, St. Jude Children’s Research Hospital , Memphis, TN 38105
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- Robert Rutschman
- Department of Infectious Diseases, St. Jude Children’s Research Hospital , Memphis, TN 38105
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- Roland Lang
- Department of Infectious Diseases, St. Jude Children’s Research Hospital , Memphis, TN 38105
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- Alessandra Pernis
- Department of Medicine, Columbia University , New York, NY 10032
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- Stephanie S Watowich
- Department of Immunology, M. D. Anderson Cancer Center , Houston, TX 77030
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- Peter J Murray
- Department of Infectious Diseases, St. Jude Children’s Research Hospital , Memphis, TN 38105
書誌事項
- 公開日
- 2004-06
- 権利情報
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- https://academic.oup.com/pages/standard-publication-reuse-rights
- DOI
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- 10.4049/jimmunol.172.12.7565
- 公開者
- Oxford University Press (OUP)
この論文をさがす
説明
<jats:title>Abstract</jats:title> <jats:p>Arginase I expression in the liver must remain constant throughout life to eliminate excess nitrogen via the urea cycle. In contrast, arginase I expression in macrophages is silent until signals from Th2 cytokines such as IL-4 and IL-13 are received and the mRNA is then induced four to five orders of magnitude. Arginase I is hypothesized to play a regulatory and potentially pathogenic role in diseases such as asthma, parasitic, bacterial, and worm infections by modulating NO levels and promoting fibrosis. We show that Th2-inducible arginase I expression in mouse macrophages is controlled by an enhancer that lies −3 kb from the basal promoter. PU.1, IL-4-induced STAT6, and C/EBPβ assemble at the enhancer and await the effect of another STAT6-regulated protein(s) that must be synthesized de novo. Identification of a powerful extrahepatic regulatory enhancer for arginase I provides potential to manipulate arginase I activity in immune cells while sparing liver urea cycle function.</jats:p>
収録刊行物
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- The Journal of Immunology
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The Journal of Immunology 172 (12), 7565-7573, 2004-06
Oxford University Press (OUP)