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Inhibitor of nuclear factor-kappaB alpha derepresses hypoxia-inducible factor-1 during moderate hypoxia by sequestering factor inhibiting hypoxia-inducible factor from hypoxia-inducible factor 1α
DC Field | Value | Language |
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dc.contributor.author | Shin, Dong Hoon | - |
dc.contributor.author | Li, Shan Hua | - |
dc.contributor.author | Yang, Seung-Won | - |
dc.contributor.author | Lee, Byung Lan | - |
dc.contributor.author | Park, Jong-Wan | - |
dc.contributor.author | Lee, Myung Kyu | - |
dc.date.accessioned | 2012-07-09T08:33:11Z | - |
dc.date.available | 2012-07-09T08:33:11Z | - |
dc.date.issued | 2009-07 | - |
dc.identifier.citation | FEBS JOURNAL; Vol.276(13); 3470-3480 | ko_KR |
dc.identifier.issn | 1742-464X | - |
dc.identifier.uri | https://hdl.handle.net/10371/78668 | - |
dc.description.abstract | Hypoxia and inflammation often develop concurrently in numerous diseases, and both hypoxia-inducible factor (HIF)-1 alpha and nuclear factor-kappaB (NF-kappa B) are key transcription factors of stress response genes. An NF-kappa B inhibitor, inhibitor of NF-kappa Ba (I kappa B alpha), was found to interact with factor inhibiting HIF (FIH) and to be hydroxylated by FIH. However, FIH did not functionally regulate I kappa B alpha, and the consequence of the FIH-I kappa B alpha interaction thus remains uncertain. In the present study, we tested the possibility that I kappa B alpha regulates FIH. FIH-I kappa B alpha binding was confirmed by yeast two-hybrid and coimmunoprecipitation analyses. Functionally, I kappa B alpha expression further enhanced the transcriptional activity of HIF-1 alpha under hypoxic conditions. Furthermore, I kappa B alpha knockdown repressed HIF-1 alpha activity. Mechanistically, I kappa B alpha derepressed HIF-1 alpha activity by inhibiting the FIH-mediated Asn803 hydroxylation of HIF-1 alpha. It was also found that I kappa B alpha activated HIF-1 alpha by sequestering FIH from HIF-1 alpha. However, the effect of I kappa B alpha on HIF-1 alpha activity was only observed in atmospheres containing 1% or more of oxygen. After tumor necrosis factor-alpha treatment, I kappa B alpha downregulation, Asn803 hydroxylation and HIF-1 alpha inactivation all occurred up to 8 h, but subsided later. On the basis of these results, we propose that I kappa B alpha plays a positive regulatory role during HIF-1-mediated gene expression. Therefore, I kappa B alpha, owing to its interactions with NF-kappa B and HIF-1 alpha, may play a pivotal role in the crosstalk between the molecular events that underlie inflammatory and hypoxic responses. | ko_KR |
dc.language.iso | en | ko_KR |
dc.publisher | WILEY-BLACKWELL PUBLISHING, INC | ko_KR |
dc.subject | factor inhibiting hypoxia-inducible factor (FIH) | ko_KR |
dc.subject | protein interaction | ko_KR |
dc.subject | nuclear factor-kappaB (NF-κB) | ko_KR |
dc.subject | hypoxia-inducible factor-1 (HIF-1) | ko_KR |
dc.subject | IκBα | ko_KR |
dc.title | Inhibitor of nuclear factor-kappaB alpha derepresses hypoxia-inducible factor-1 during moderate hypoxia by sequestering factor inhibiting hypoxia-inducible factor from hypoxia-inducible factor 1α | ko_KR |
dc.type | Article | ko_KR |
dc.contributor.AlternativeAuthor | 신동훈 | - |
dc.contributor.AlternativeAuthor | 양승원 | - |
dc.contributor.AlternativeAuthor | 이병란 | - |
dc.contributor.AlternativeAuthor | 이명규 | - |
dc.contributor.AlternativeAuthor | 박종완 | - |
dc.identifier.doi | 10.1111/j.1742-4658.2009.07069.x | - |
dc.citation.journaltitle | FEBS JOURNAL | - |
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dc.description.tc | 5 | - |
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