Calpain interactions with the protein phosphatase calcineurin in neurodegeneration

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

8 Scopus citations

Abstract

Dysregulation of intracellular Ca2+ is a major cause of neurologic dysfunction and likely plays an important role in the pathophysiology of numerous acute and chronic neurodegenerative conditions. The Ca2+-dependent protease, calpain, and the Ca2+/calmodulin (Ca2+/CaM)-dependent protein phosphatase, calci- neurin, are primary effectors of multiple deleterious functions arising from altered Ca2+ handling. Increasing evidence suggests that the calpain-dependent, irreversible conversion of calcineurin to a constitutively active phosphatase occurs in intact cellular systems as a result of injury and disease. In this chapter, a brief overview of calpain and calcineurin functions in nervous tissue is given, followed by a more in-depth discussion of calpain/calcineurin interactions in vitro and in vivo. Particular emphasis is placed on recent studies that have identified calpain proteolysis of cal- cineurin as a key step in neurodegeneration associated with acute neurologic insults as well as chronic terminal diseases, like Alzheimer's.

Original languageEnglish
Title of host publicationRole of Proteases in Cellular Dysfunction
Pages17-45
Number of pages29
ISBN (Electronic)9781461490999
DOIs
StatePublished - Jan 1 2014

Keywords

  • Alzheimer's
  • Calcium
  • Dementia
  • Ischemia
  • Neurodegeneration
  • Phosphatase
  • Protease

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology (all)

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