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NAIP interacts with hippocalcin and protects against calcium-induced cell death through caspase-3 dependent and independent pathways
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Neuroscience.
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2000 In: EMBO J., Vol. 19, 3597-3607 p.Article in journal (Refereed) Published
Place, publisher, year, edition, pages
2000. Vol. 19, 3597-3607 p.
URN: urn:nbn:se:uu:diva-89655OAI: oai:DiVA.org:uu-89655DiVA: diva2:161320
Available from: 2002-02-15 Created: 2002-02-15Bibliographically approved
In thesis
1. Anti-Apoptotic Proteins in Nerve Cell Survival and Neurodegeneration
Open this publication in new window or tab >>Anti-Apoptotic Proteins in Nerve Cell Survival and Neurodegeneration
2002 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Apoptosis is a genetically regulated cell death program, which shows distinct morphological characteristics. It takes place during neuronal development and in some neurodegenerative diseases. During apoptosis, the intracellular proteins are degraded by various caspases, cysteine aspartases, which are regulated by pro- and anti-apoptotic signals. This thesis elucidates the role of anti-apoptotic proteins in nerve cell survival and neurodegeneration. Studies have focused on Bcl-2 family members and Inhibitor of Apoptosis Proteins (IAP).

XIAP and RIAP-2 are IAP proteins, which are expressed by neurons in the central nervous system. Kainic acid, a glutamate receptor agonist that induces seizures, increased XIAP immunoreactivity in rat hippocampus, whereas RIAP-2 expression in the same time decreased in degenerating neurons. Both XIAP and RIAP-2 were absent in dying neurons indicating that these proteins have a protective role in kainic acid induced neurodegeneration.

NAIP, another IAP family member, was shown to interact with the calcium binding protein Hippocalcin using the yeast two-hybrid system and immunoprecipitation experiments. Hippocalcin-NAIP interaction increased motoneuron survival in caspase-3 independent and dependent manners.

The anti-apoptotic Bcl-2 proteins, Bcl-2 and Bcl-x, were studied using cultured neurons and human neuronal progenitor cells. In the progenitor cells, Bcl-2 overexpression enhanced cell survival and induced downregulation of Caspase-2 (ICH-1) and caspase-3 (YAMA/CPP32). These results suggest a novel mechanism for the action of Bcl-2.

Estrogen was shown to inhibit death of cultured dorsal root ganglion neurons (DRG) after nerve growth factor withdrawal. The hormone increased the levels of Bcl-x, which may explain the known neuroprotective function of estrogen.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2002. 65 p.
Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 0282-7476 ; 1120
Neurosciences, neuronal cell death, XIAP, RIAP-2, Hippocalcin, Bcl-2, Bcl-X, kainic acid, DRG, estrogen, Neurovetenskap
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Research subject
Developmental Neurosciences
urn:nbn:se:uu:diva-1752 (URN)91-554-5230-2 (ISBN)
Public defence
2002-03-08, Uppsala Biomedical Centre (BMC), lecture room B22, Uppsala, 09:15
Available from: 2002-02-15 Created: 2002-02-15Bibliographically approved

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