Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8295375 | Biochemical and Biophysical Research Communications | 2018 | 37 Pages |
Abstract
Absence of the GluN2C subunit from the N-methyl-D-aspartate pool of ion channels diminished neuroedema in a murine model of ischemic stroke. The penumbral neurons of the core infarct of the GluN2C-/- mice showed diminished cytoskeletal disruption, decreased tauopathy, and increased phosphorylation of the pro-survival CREB molecule compared to WT mice. Thus, the GluN2C subunit impairs stroke-mediated neurological deficits, thereby, making the GluN2C subunit an attractive therapeutic target.177
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Authors
Adam Holmes, Ning Zhou, Deborah L. Donahue, Rashna Balsara, Francis J. Castellino,