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A secreted form of human ADAM9 has an alpha-secretase activity for APP

Nika Hotoda1, Hisashi Koike, Noboru Sasagawa

  • 1Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro-ku, Tokyo 153-8902, Japan.

Insights

A novel short form of ADAM9 (hADAM9s) was identified and found to possess alpha-secretase-like activity. This discovery suggests a new therapeutic strategy for reducing amyloid-beta peptide levels by activating extracellular ADAM9.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Neuroscience

Background:

  • ADAM9 (ADAM metallopeptidase domain 9) is a metalloprotease involved in cellular functions.
  • The ADAM family plays roles in cell-cell fusion and intracellular signaling.

Purpose of the Study:

  • To clone and characterize a novel, shorter form of human ADAM9 (hADAM9s).
  • To investigate the enzymatic activity and potential therapeutic applications of hADAM9s, particularly concerning amyloid precursor protein (APP) processing.

Main Methods:

  • Cloning of the novel hADAM9s variant.
  • Expression of hADAM9s in transfected COS cells and detection of its secretion.
  • RT-PCR analysis to determine hADAM9s mRNA expression in various human tissues.
  • Co-expression of hADAM9s with APP in COS cells, followed by phorbol ester treatment to assess APP cleavage.

Main Results:

  • A novel secreted form of human ADAM9, hADAM9s, was successfully cloned and expressed.
  • hADAM9s mRNA was detected in multiple human tissues, including brain and liver.
  • hADAM9s demonstrated exclusive cleavage of APP at the alpha-secretory site, indicating alpha-secretase-like activity.
  • This cleavage occurs at the plasma membrane, suggesting a non-amyloidogenic pathway for APP processing.

Conclusions:

  • hADAM9s exhibits alpha-secretase-like activity, cleaving APP at the non-amyloidogenic site.
  • Extracellular activation of ADAM9 presents a potential therapeutic strategy to reduce amyloid-beta (Abeta) peptide accumulation.
  • This finding opens new avenues for therapeutic interventions in conditions associated with Abeta pathology.

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