Oxidant-regulation of Gene Expression in the Chronically Inflamed Intestine

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著者

    • JOURD'HEUIL David
    • Department of Molecular and Cellular Physiology, Louisiana State University Medical Center Department of Molecular and Cellular Physiology, Louisiana State University Medical Center
    • 守瀬 善一 MORISE Zenichi
    • Department of Molecular and Cellular Physiology, Louisiana State University Medical Center Department of Molecular and Cellular Physiology, Louisiana State University Medical Center
    • CONNER Elaine M
    • Department of Molecular and Cellular Physiology, Louisiana State University Medical Center Department of Molecular and Cellular Physiology, Louisiana State University Medical Center
    • 黒瀬 巌 KUROSE Iwao
    • Department of Molecular and Cellular Physiology, Louisiana State University Medical Center Department of Molecular and Cellular Physiology, Louisiana State University Medical Center
    • GRISHAM Matthew B
    • Department of Molecular and Cellular Physiology, Louisiana State University Medical Center Department of Molecular and Cellular Physiology, Louisiana State University Medical Center

抄録

It is becoming increasingly apparent that the chronic gut inflammation observed in the idiopathic inflammatory bowel diseases (e.g. ulcerative colitis, Crohn's disease) is associated with enhanced production of leukocyte-derived oxidants. Oxidants such as hydrogen peroxide are known to activate certain transcription factors such as nuclear transcription factor x beta. Nuclear transcription factor kB (NF-KB) is a ubiquitous transcription factor and pleiotropic regulator of numerous genes involved in the immune and inflammatory responses. This transcription factor is activated via the selective phosphorylation, ubiquination and degradation of its inhibitor protein I-kB thereby allowing translocation of NF-KB into the nucleus where it upregulates the transcription of a variety of adhesion molecules (e.g. ICAM-1, VCAM-1), cytokines (TNF, IL-1, IL-6) and enzymes (iNOS). The proteolytic degradation of the post-translationally modified I-KB is known to be mediated by the 26S proteasome complex. Based upon work from our laboratory, we propose that inhibition of NF-KB activation produces significant antiinflammatory activity which may be mediated by the inhibition of transcription of certain pro-inflammatory mediators and adhesion molecules.

収録刊行物

  • Keio journal of medicine  

    Keio journal of medicine 46(1), 10-15, 1997-03-01 

    The Keio Journal of Medicine

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各種コード

  • NII論文ID(NAID)
    10021987497
  • NII書誌ID(NCID)
    AA00710216
  • 本文言語コード
    ENG
  • 資料種別
    REV
  • ISSN
    00229717
  • データ提供元
    CJP書誌  J-STAGE 
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