HECT E3s and human disease
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  • 作者:Martin Scheffner (1)
    Olivier Staub (2)
  • 刊名:BMC Biochemistry
  • 出版年:2007
  • 出版时间:November 2007
  • 年:2007
  • 卷:8
  • 期:1-supp
  • 全文大小:982KB
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  • 作者单位:Martin Scheffner (1)
    Olivier Staub (2)

    1. Department of Biology, University of Konstanz, 78457, Konstanz, Germany
    2. Department of Pharmacology and Toxicology, University of Lausanne, Rue du Bugnon 27, 1005, Lausanne, Switzerland
文摘
In a simplified view, members of the HECT E3 family have a modular structure consisting of the C-terminal HECT domain, which is catalytically involved in the attachment of ubiquitin to substrate proteins, and N-terminal extensions of variable length and sequence that mediate the substrate specificity of the respective HECT E3. Although the physiologically relevant substrates of most HECT E3s have remained elusive, it is becoming increasingly clear that HECT E3s play an important role in sporadic and hereditary human diseases including cancer, cardiovascular (Liddle's syndrome) and neurological (Angelman syndrome) disorders, and/or in disease-relevant processes including bone homeostasis, immune response and retroviral budding. Thus, molecular approaches to target the activity of distinct HECT E3s, regulators thereof, and/or of HECT E3 substrates could prove valuable in the treatment of the respective diseases. Publication history: Republished from Current BioData's Targeted Proteins database (TPdb; http://www.targetedproteinsdb.com).

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