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GSK-3α/β kinases and amyloid production in vivo

Author

Listed:
  • Tomasz Jaworski

    (Experimental Genetics Group)

  • Ilse Dewachter

    (Experimental Genetics Group)

  • Benoit Lechat

    (Experimental Genetics Group)

  • Maarten Gees

    (Experimental Genetics Group)

  • Anna Kremer

    (Experimental Genetics Group)

  • David Demedts

    (Experimental Genetics Group)

  • Peter Borghgraef

    (Experimental Genetics Group)

  • Herman Devijver

    (Experimental Genetics Group)

  • Seb Kügler

    (Georg-August-University)

  • Satish Patel

    (Samuel Lunenfeld Research Institute, Mount Sinai Hospital)

  • Jim R. Woodgett

    (Samuel Lunenfeld Research Institute, Mount Sinai Hospital)

  • Fred Van Leuven

    (Experimental Genetics Group)

Abstract

Arising from C. J. Phiel, C. A. Wilson, V. M.-Y. Lee & P. S. Klein Nature 423, 435–439 (2003)10.1038/nature01640 A major unresolved issue in Alzheimer’s disease is identifying the mechanisms that regulate proteolytic processing of amyloid precursor protein (APP)—glycogen synthase kinase-3 (GSK-3) isozymes are thought to be important in this regulation. Phiel et al.1 proposed that GSK-3α, but not GSK-3β, controls production of amyloid1. We analysed the proteolytic processing of mouse and human APP in mouse brain in vivo in five different genetic and viral models. Our data do not yield evidence for either GSK-3α-mediated or GSK-3β-mediated control of APP processing in brain in vivo.

Suggested Citation

  • Tomasz Jaworski & Ilse Dewachter & Benoit Lechat & Maarten Gees & Anna Kremer & David Demedts & Peter Borghgraef & Herman Devijver & Seb Kügler & Satish Patel & Jim R. Woodgett & Fred Van Leuven, 2011. "GSK-3α/β kinases and amyloid production in vivo," Nature, Nature, vol. 480(7376), pages 4-5, December.
    • Handle: RePEc:nat:nature:v:480:y:2011:i:7376:d:10.1038_nature10615
    DOI: 10.1038/nature10615
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