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Gerber H, Wu F, Dimitrov M, et al. Zinc and Copper Differentially Modulate Amyloid Precursor Protein Processing by γ-Secretase and Amyloid-β Peptide Production. J Biol Chem. 2017;292(9):3751-3767doi: 10.1074/jbc.M116.754101.
Gerber, H., Wu, F., Dimitrov, M., Garcia Osuna, G. M., & Fraering, P. C. (2017). Zinc and Copper Differentially Modulate Amyloid Precursor Protein Processing by γ-Secretase and Amyloid-β Peptide Production. The Journal of biological chemistry, 292(9), 3751-3767. https://doi.org/10.1074/jbc.M116.754101
Gerber, Hermeto, et al. "Zinc and Copper Differentially Modulate Amyloid Precursor Protein Processing by γ-Secretase and Amyloid-β Peptide Production." The Journal of biological chemistry vol. 292,9 (2017): 3751-3767. doi: https://doi.org/10.1074/jbc.M116.754101
Gerber H, Wu F, Dimitrov M, Garcia Osuna GM, Fraering PC. Zinc and Copper Differentially Modulate Amyloid Precursor Protein Processing by γ-Secretase and Amyloid-β Peptide Production. J Biol Chem. 2017 Mar 03;292(9):3751-3767. doi: 10.1074/jbc.M116.754101. Epub 2017 Jan 17. PMID: 28096459; PMCID: PMC5339758.
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J Biol Chem. 2017 Mar 03;292(9):3751-3767. doi: 10.1074/jbc.M116.754101. Epub 2017 Jan 17.

Zinc and Copper Differentially Modulate Amyloid Precursor Protein Processing by γ-Secretase and Amyloid-β Peptide Production.

The Journal of biological chemistry

Hermeto Gerber, Fang Wu, Mitko Dimitrov, Guillermo M Garcia Osuna, Patrick C Fraering

Affiliations

  1. From the Foundation Eclosion, CH-1228 Plan-Les-Ouates, and Campus Biotech Innovation Park, CH-1202 Geneva, Switzerland.
  2. the Brain Mind Institute and School of Life Sciences, Swiss Federal Institute of Technology (EPFL), CH-1015 Lausanne, Switzerland.
  3. the Department of Biology, University of Fribourg, CH-1700 Fribourg, Switzerland, and.
  4. the Key Laboratory of Systems Biomedicine, Ministry of Education, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, 200240 Shanghai, China.
  5. From the Foundation Eclosion, CH-1228 Plan-Les-Ouates, and Campus Biotech Innovation Park, CH-1202 Geneva, Switzerland, [email protected].

PMID: 28096459 PMCID: PMC5339758 DOI: 10.1074/jbc.M116.754101

Abstract

Recent evidence suggests involvement of biometal homeostasis in the pathological mechanisms in Alzheimer's disease (AD). For example, increased intracellular copper or zinc has been linked to a reduction in secreted levels of the AD-causing amyloid-β peptide (Aβ). However, little is known about whether these biometals modulate the generation of Aβ. In the present study we demonstrate in both cell-free and cell-based assays that zinc and copper regulate Aβ production by distinct molecular mechanisms affecting the processing by γ-secretase of its Aβ precursor protein substrate APP-C99. We found that Zn

© 2017 by The American Society for Biochemistry and Molecular Biology, Inc.

Keywords: Alzheimer disease; amyloid precursor protein (APP); amyloid-β (AB); biometals; copper; intramembrane proteolysis; neurodegeneration; zinc

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