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Expression of seizure-related PTZ-17 is induced by potassium deprivation in cerebellar granule cells.

作者信息

Roschier M, Kuusisto E, Kyrylenko S, Salminen A

机构信息

Department of Neuroscience and Neurology, University of Kuopio, Kuopio, FIN-70211, USA.

出版信息

Biochem Biophys Res Commun. 1998 Nov 9;252(1):10-3. doi: 10.1006/bbrc.1998.9589.

DOI:10.1006/bbrc.1998.9589
PMID:9813137
Abstract

The aim of this study was to identify changes in gene expression during neuronal apoptosis using the differential display (DD) technique. Potassium deprivation was used to induce neuronal apoptosis in cultured rat cerebellar granule cells. DD analysis of about 1600 transcripts resulted in 8 cDNA clones that confirmed differential expression in a slot blot analysis. One of these clones was homologous to the 3' end of seizure-related PTZ-17 RNA. Northern blot analysis showed a marked upregulation of a 2.2 kb RNA 24 hours after potassium withdrawal. This upregulation was prevented by the RNA synthesis inhibitor actinomycin D. The increase in PTZ-17 expression was specific for potassium deprivation induced apoptosis, since the other apoptosis inducers, okadaic acid and staurosporine, did not affect PTZ-17 expression. The level of PTZ-17 RNA was not significantly affected by aging in rat cerebellum. Our data suggest that the upregulation of the PTZ-17 RNA is a part of the steps leading to apoptosis during potassium deprivation in cerebellar granule cells.

摘要

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