Life and Death under the ER Stress Condition

• Nishitoh Hideki

  Center of Excellence (COE) Program for Research on Molecular Destruction and Reconstruction of Tooth and Bone, Oral and Maxillofacial Surgery, Graduate School, Tokyo Medical and Dental University

抄録

The endoplasmic reticulum (ER) regulates protein synthesis, folding and trafficking, cellular responses to stress, and intracellular calcium (Ca²⁺) levels. Accumulation of misfolded proteins and alterations in Ca²⁺ homeostasis in the ER cause ER stress. Eukaryotic cells possess at least three different mechanisms to adapt to ER stress and thereby survive : (1) transcriptional activation of genes encoding ER-resident chaperones, (2) translational attenuation which limits further accumulation of misfolded proteins, and (3) the ER-associated degradation (ERAD) pathway, which restores the folding capacity. If the cells are exposed to prolonged and/or strong ER stress, they are destroyed by apoptosis. Recent evidence has indicated that ER stress signaling pathways are mediated by several intracellular signaling pathways and play an important role in the pathogenesis of conformational diseases. The main purpose of this review is to summarize current knowledge about the ER stress signaling pathways and their involvement in the pathogenesis of diseases.

収録刊行物

• Journal of Oral Biosciences

  Journal of Oral Biosciences 46 (4), 259-269, 2004

  歯科基礎医学会

キーワード

• ER stress
• apoptosis
• ASK1
• JNK
• conformational diseases

詳細情報

• CRID: 1390282680189617920
• NII論文ID: 110003166647
• NII書誌ID: AA11896386
• DOI: 10.2330/joralbiosci.46.259
• ISSN: 18803865
• ISSN: 13490079
• Web Site: https://search.jamas.or.jp/link/ui/2004303285
• 本文言語コード: en
• データソース種別:
  • JaLC
  • Crossref
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可