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    FEBS Lett. 2009 Nov 19;583(22):3577-81. Epub 2009 Oct 17.

    Differential regulation by ATP versus ADP further links CaMKII aggregation to ischemic conditions.

    Vest RS, O'Leary H, Bayer KU.

    Source

    Department of Pharmacology, University of Colorado Denver, Aurora, CO 80045, United States.

    Abstract

    CaMKII, a major mediator of synaptic plasticity, forms extra-synaptic clusters under ischemic conditions. This study further supports self-aggregation of CaMKII holoenzymes as the underlying mechanism. Aggregation in vitro was promoted by mimicking ischemic conditions: low pH (6.8 or less), Ca(2+) (and calmodulin), and low ATP and/or high ADP concentration. Mutational analysis showed that high ATP prevented aggregation by a mechanism involving T286 auto-phosphorylation, and indicated requirement for nucleotide binding but not auto-phosphorylation also for extra-synaptic clustering within neurons. These results clarify a previously apparent paradox in the nucleotide and phosphorylation requirement of aggregation, and support a mechanism that involves inter-holoenzyme T286-region/T-site interaction.

    PMID:
    19840793
    [PubMed - indexed for MEDLINE]
    PMCID:
    PMC2790910
    Free PMC Article

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