Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10956930 | Molecular and Cellular Neuroscience | 2005 | 11 Pages |
Abstract
Hippocalcin is a neuronal calcium binding protein, but its physiological function in brain is unknown. We show here that hippocampal neurons from hippocalcin-deficient mice are more vulnerable to degeneration, particularly using thapsigargin, elevating intracellular calcium. Caspase-12 was activated in neurons lacking hippocalcin, while calpain was unchanged. Neuronal viability was accompanied by endoplasmic reticulum (ER) stress and a change in the relative induction of the ER chaperone, BiP/GRP78. Neuronal apoptosis inhibitor protein (NAIP), known to interact with hippocalcin, was not altered, but hippocampal neurons from gene-deleted mice were more sensitive to excitotoxicity caused by kainic acid. In addition, an age-dependent increase in neurodegeneration occurred in the gene-deleted mice, showing that hippocalcin contributes to neuronal viability during aging.
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Authors
Laura Korhonen, Inga Hansson, Jyrki P. Kukkonen, Karin Brännvall, Masaaki Kobayashi, Ken Takamatsu, Dan Lindholm,