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Pathways of Neuronal Cell Death Induced by Proteasomal Inhibition

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Book cover The Proteasome in Neurodegeneration

Abstract

Acute proteasomal inhibition of sufficient severity in cultured primary neurons leads to the upregulation of a number of potentially deleterious proteins, such as p53 or those related to cell cycle control. Accumulation of misfolded or oxidized proteins may also have detrimental effects. Such changes lead in most cases to the activation of the “intrinsic” apoptotic pathway with participation of the mitochondria. Specific pro-apoptotic components of this intrinsic pathway, such as BH3-only members of the bcl-2 family, may also accumulate and play a role in neuronal death. The question of whether similar pathways are involved in vivo in the setting of long-standing inhibition of the proteasome, such as may occur in certain neurodegenerative conditions, awaits the generation of appropriate animal models.

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Authors and Affiliations

  1. Department of Psychiatry, Max-Planck-Institut für Psychiatrie München, Munich, Germany

    Dr. Isabelle Lang-Rollin

  2. Section of Neurobiology, Institute for Biomedical Research, Academy of Athens, Athens, Greece

    Dr. Leonidas Stefanis

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  1. Dr. Isabelle Lang-Rollin
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  2. Dr. Leonidas Stefanis
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  1. Institute of Biomedical Research of the Academy of Athens, Athens, Greece

    Leonidas Stefanis

  2. Sanders-Brown Center on Aging Department of Anatomy and Neurobiology, University of Kentucky, KY, USA

    Jeffrey N. Keller

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Lang-Rollin, I., Stefanis, L. (2006). Pathways of Neuronal Cell Death Induced by Proteasomal Inhibition. In: Stefanis, L., Keller, J.N. (eds) The Proteasome in Neurodegeneration. Springer, Boston, MA. https://doi.org/10.1007/0-387-28500-8_9

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