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- Qiutang Li
- Salk Institute, La Jolla, CA 92037, USA.
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- Daniel Van Antwerp
- Salk Institute, La Jolla, CA 92037, USA.
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- Frank Mercurio
- Signal Pharmaceuticals, San Diego, CA 92121, USA.
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- Kuo-Fen Lee
- Salk Institute, La Jolla, CA 92037, USA.
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- Inder M. Verma
- Salk Institute, La Jolla, CA 92037, USA.
書誌事項
- 公開日
- 1999-04-09
- DOI
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- 10.1126/science.284.5412.321
- 公開者
- American Association for the Advancement of Science (AAAS)
この論文をさがす
説明
<jats:p> Phosphorylation of inhibitor of kappa B (IκB) proteins is an important step in the activation of the transcription nuclear factor kappa B (NF-κB) and requires two IκB kinases, IKK1 (IKKα) and IKK2 (IKKβ). Mice that are devoid of the IKK2 gene had extensive liver damage from apoptosis and died as embryos, but these mice could be rescued by the inactivation of the gene encoding tumor necrosis factor receptor 1. Mouse embryonic fibroblast cells that were isolated from IKK2 <jats:sup>–/–</jats:sup> embryos showed a marked reduction in tumor necrosis factor–α (TNF-α)– and interleukin-1α–induced NF-κB activity and an enhanced apoptosis in response to TNF-α. IKK1 associated with NF-κB essential modulator (IKKγ/IKKAP1), another component of the IKK complex. These results show that IKK2 is essential for mouse development and cannot be substituted with IKK1. </jats:p>
収録刊行物
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- Science
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Science 284 (5412), 321-325, 1999-04-09
American Association for the Advancement of Science (AAAS)
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詳細情報 詳細情報について
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- CRID
- 1364233269242543104
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- NII論文ID
- 80011039453
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- ISSN
- 10959203
- 00368075
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- データソース種別
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- Crossref
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