Cholinergic agonists and interleukin 1 regulate processing and secretion of the Alzheimer beta/A4 amyloid protein precursor.

DOI Web Site 被引用文献7件
  • J D Buxbaum
    Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10021.
  • M Oishi
    Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10021.
  • H I Chen
    Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10021.
  • R Pinkas-Kramarski
    Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10021.
  • E A Jaffe
    Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10021.
  • S E Gandy
    Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10021.
  • P Greengard
    Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10021.

書誌事項

公開日
1992-11
DOI
  • 10.1073/pnas.89.21.10075
公開者
Proceedings of the National Academy of Sciences

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説明

<jats:p>Activation of protein kinase C by phorbol esters is known to accelerate the processing and secretion of the beta/A4 amyloid protein precursor. We have now examined various first messengers that increase protein kinase C activity of target cells for their ability to affect beta/A4 amyloid protein precursor metabolism. Acetylcholine and interleukin 1, which are altered in Alzheimer disease, were shown to increase processing of the beta/A4 amyloid protein precursor via the secretory cleavage pathway. Cholinergic agonists stimulated secretion in human glioma and neuroblastoma cells as well as in PC12 cells transfected with the M1 receptor, while interleukin 1 stimulated secretion in human endothelial and glioma cells.</jats:p>

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