Cyclin-dependent protein kinase 5 activity increases in rat brain following ischemia

Sherril L. Green, Kristen S. Kulp, Philip R Vulliet

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

Cyclin-dependent kinase 5 (CDK5) is the 34 kDa catalytic subunit of a recently characterized neuronal cdc2-like protein kinase which appears to be involved in regulation of the neurocytoskeleton. Using the rat postdecapitative model, the effect of brain ischemia on histone H1 and tan protein CDK5 phosphorylating activity was examined. Histone H1 kinase activity increased in both cytosolic and particulate fractions of the hippocampus and neocortex after 5 min and 15 min of ischemia, then declined to control levels. CDK5 tau protein phosphorylating activity increased after 15 min ischemia; however, no electrophoretic shifts or changes in radiodensity of the tau bands were observed autoradiographically. On Western blot analysis, the CDK5 protein band did not change after 25 min ischemia, despite the increase and subsequent decline in enzyme activity. These data demonstrate a postischemic increase in CDK5 activity, an associated increase in CDK5 tau phosphorylating activity and a decline in activity in the absence of massive proteolysis. CDK5 appears to play a role in the events associated with neuronal response to ischemic injury.

Original languageEnglish (US)
Pages (from-to)617-623
Number of pages7
JournalNeurochemistry International
Volume31
Issue number4
DOIs
StatePublished - Oct 1997

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Cyclin-Dependent Kinase 5
Cyclin-Dependent Kinases
Brain Ischemia
Ischemia
tau Proteins
Neocortex
Histones
Proteolysis
Hippocampus
Catalytic Domain
Proteins
Western Blotting

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Cellular and Molecular Neuroscience

Cite this

Cyclin-dependent protein kinase 5 activity increases in rat brain following ischemia. / Green, Sherril L.; Kulp, Kristen S.; Vulliet, Philip R.

In: Neurochemistry International, Vol. 31, No. 4, 10.1997, p. 617-623.

Research output: Contribution to journalArticle

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