Calpain interactions with the protein phosphatase calcineurin in neurodegeneration

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

8 Scopus citations


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
Number of pages29
ISBN (Electronic)9781461490999
StatePublished - Jan 1 2014


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

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology (all)


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