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Hippocalcin protects against caspase-12-induced and age-dependent neuronal degeneration

Korhonen, Laura (author)
Linköpings universitet,Uppsala universitet,Institutionen för neurovetenskap,Neurobiologi,Lindholm
Hansson, Inga (author)
Uppsala universitet,Institutionen för neurovetenskap,Neurobiologi,Lindholm
Kukkonen, J P (author)
Uppsala universitet,Institutionen för neurovetenskap,Fysiologi,Kukkonen
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Brännvall, Karin (author)
Uppsala universitet,Institutionen för neurovetenskap,Neurobiologi,Lindholm
Kobayashi, M (author)
Takamatsu, K (author)
Lindholm, Dan (author)
Uppsala universitet,Institutionen för neurovetenskap,Neurobiologi,Lindholm
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 (creator_code:org_t)
Uppsala Univ, Ctr Biomed, Dept Neurosci, Neurobiol Unit, S-75123 Uppsala, Sweden. Uppsala Univ, Ctr Biomed, Dept Neurosci, Unit Physiol, S-75123 Uppsala, Sweden. Toho Univ, Sch Med, Dept Physiol, Ohta Ku, Tokyo 1438540, Japan. Minerva Med Res Inst, Biomedicum Helsinki, FIN-00290 Helsinki, Finland. ACADEMIC PRESS INC ELSEVIER SCIENCE, 2005
2005
English.
In: Molecular and Cellular Neuroscience. - Uppsala Univ, Ctr Biomed, Dept Neurosci, Neurobiol Unit, S-75123 Uppsala, Sweden. Uppsala Univ, Ctr Biomed, Dept Neurosci, Unit Physiol, S-75123 Uppsala, Sweden. Toho Univ, Sch Med, Dept Physiol, Ohta Ku, Tokyo 1438540, Japan. Minerva Med Res Inst, Biomedicum Helsinki, FIN-00290 Helsinki, Finland. : ACADEMIC PRESS INC ELSEVIER SCIENCE. - 1044-7431 .- 1095-9327. ; 28:1, s. 85-95
  • Journal article (peer-reviewed)
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  • 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. (C) 2004 Elsevier Inc. All rights reserved.

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